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human leukemic cell line k562 cells  (ATCC)


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    Structured Review

    ATCC human leukemic cell line k562 cells
    Elevated expression of lncRNA ZFAS1 and STAT3 in imatinib-resistant (IM-R) CML patient samples and IM-R <t>K562</t> cell line. (A, B) Relative expressions of ZFAS1 and STAT3 in peripheral blood cells from imatinib-resistant (IM-R, n=30) and imatinib-sensitive (IM-S, n=30) CML patients. (C) Correlation analysis between ZFAS1 and STAT3 in CML patients samples. (D, E) Expression levels of lncRNA ZFAS1 and STAT3 in IM-R and IM-S K562 cells. Data are presented as mean ± SD. *** p <0.001 vs . IM-S.
    Human Leukemic Cell Line K562 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 11229 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human leukemic cell line k562 cells/product/ATCC
    Average 99 stars, based on 11229 article reviews
    human leukemic cell line k562 cells - by Bioz Stars, 2026-02
    99/100 stars

    Images

    1) Product Images from "ZFAS1/STAT3 axis modulates imatinib resistance of chronic myeloid leukemia cells through glucose metabolism reprogramming"

    Article Title: ZFAS1/STAT3 axis modulates imatinib resistance of chronic myeloid leukemia cells through glucose metabolism reprogramming

    Journal: Frontiers in Oncology

    doi: 10.3389/fonc.2025.1603060

    Elevated expression of lncRNA ZFAS1 and STAT3 in imatinib-resistant (IM-R) CML patient samples and IM-R K562 cell line. (A, B) Relative expressions of ZFAS1 and STAT3 in peripheral blood cells from imatinib-resistant (IM-R, n=30) and imatinib-sensitive (IM-S, n=30) CML patients. (C) Correlation analysis between ZFAS1 and STAT3 in CML patients samples. (D, E) Expression levels of lncRNA ZFAS1 and STAT3 in IM-R and IM-S K562 cells. Data are presented as mean ± SD. *** p <0.001 vs . IM-S.
    Figure Legend Snippet: Elevated expression of lncRNA ZFAS1 and STAT3 in imatinib-resistant (IM-R) CML patient samples and IM-R K562 cell line. (A, B) Relative expressions of ZFAS1 and STAT3 in peripheral blood cells from imatinib-resistant (IM-R, n=30) and imatinib-sensitive (IM-S, n=30) CML patients. (C) Correlation analysis between ZFAS1 and STAT3 in CML patients samples. (D, E) Expression levels of lncRNA ZFAS1 and STAT3 in IM-R and IM-S K562 cells. Data are presented as mean ± SD. *** p <0.001 vs . IM-S.

    Techniques Used: Expressing

    Effects of ZFAS1 knockdown on imatinib-resistant K562 cells. (A) PCR analysis showing the efficiency of ZFAS1 knockdown in IM-R K562 cells. (B) Drug sensitivity assay (CCK-8) showing relative cell viability of si-NC and si-ZFAS1 IM-R K562 cells treated with varying concentrations of IM. (C) IC 50 values of imatinib in si-ZFAS1 cells and si-NC cells. (D) Colony formation assay showing the number of colonies formed by si-NC and si-ZFAS1 IM-R K562 cells treated with or without 2 µM IM. (E) Flow cytometry analysis showing the apoptosis rate of si-NC and si-ZFAS1 IM-R K562 cells treated with 2 µM IM. Data are presented as mean ± SD. NTC: non-treated control; ** p <0.01, *** p <0.001 vs . si-NC; ### p <0.001 vs . IM+si-NC.
    Figure Legend Snippet: Effects of ZFAS1 knockdown on imatinib-resistant K562 cells. (A) PCR analysis showing the efficiency of ZFAS1 knockdown in IM-R K562 cells. (B) Drug sensitivity assay (CCK-8) showing relative cell viability of si-NC and si-ZFAS1 IM-R K562 cells treated with varying concentrations of IM. (C) IC 50 values of imatinib in si-ZFAS1 cells and si-NC cells. (D) Colony formation assay showing the number of colonies formed by si-NC and si-ZFAS1 IM-R K562 cells treated with or without 2 µM IM. (E) Flow cytometry analysis showing the apoptosis rate of si-NC and si-ZFAS1 IM-R K562 cells treated with 2 µM IM. Data are presented as mean ± SD. NTC: non-treated control; ** p <0.01, *** p <0.001 vs . si-NC; ### p <0.001 vs . IM+si-NC.

    Techniques Used: Knockdown, Sensitive Assay, CCK-8 Assay, Colony Assay, Flow Cytometry, Control

    Effects of ZFAS1 knockdown on glucose metabolism in IM-R K562 cells. (A) Relative glucose uptake levels in si-NC and si-ZFAS1 IM-R K562 cells. (B) Relative lactate production in si-NC and si-ZFAS1 IM-R K562 cells. (C) Relative ATP levels in si-NC and si-ZFAS1 IM-R K562 cells. (D) Extracellular acidification rate (ECAR) in si-NC and si-ZFAS1 IM-R K562 cells. (E) Oxygen consumption rate (OCR) in si-NC and si-ZFAS1 IM-R K562 cells. (F) ECAR vs . OCR plot illustrating the metabolic shift in si-ZFAS1 IM-R K562 cells. (G) Comprehensive metabolic profile showing the impact of ZFAS1 knockdown on IM-R K562 cell metabolism. Data are presented as mean ± SD. ** p <0.01, *** p <0.001 vs . si-NC.
    Figure Legend Snippet: Effects of ZFAS1 knockdown on glucose metabolism in IM-R K562 cells. (A) Relative glucose uptake levels in si-NC and si-ZFAS1 IM-R K562 cells. (B) Relative lactate production in si-NC and si-ZFAS1 IM-R K562 cells. (C) Relative ATP levels in si-NC and si-ZFAS1 IM-R K562 cells. (D) Extracellular acidification rate (ECAR) in si-NC and si-ZFAS1 IM-R K562 cells. (E) Oxygen consumption rate (OCR) in si-NC and si-ZFAS1 IM-R K562 cells. (F) ECAR vs . OCR plot illustrating the metabolic shift in si-ZFAS1 IM-R K562 cells. (G) Comprehensive metabolic profile showing the impact of ZFAS1 knockdown on IM-R K562 cell metabolism. Data are presented as mean ± SD. ** p <0.01, *** p <0.001 vs . si-NC.

    Techniques Used: Knockdown

    STAT3 overexpression reverses the effects of ZFAS1 knockdown on imatinib sensitivity and glucose metabolism reprogramming in IM-resistant K562 cells, including si-NC+NC, si-ZFAS1+NC, and si-ZFAS1+STAT3 IM-R K562 cells. (A) Drug sensitivity assay by CCK-8 showing relative cell viability of cells treated with varying concentrations of IM. (B) IC50 values were determined via CCK-8 assay after 48 hours of imatinib treatment. (C) Relative glucose uptake levels. (D) Relative lactate production. (E) Relative ATP levels. (F) ECAR over time. (G) Glycolysis and glycolytic capacity. (H) OCR over time. (I) Summary of basal respiration and maximal respiration. ** p <0.01, *** p <0.001 vs . si-NC+NC; # p <0.05, ## p <0.01, ### p <0.001 vs . si-ZFAS1+NC.
    Figure Legend Snippet: STAT3 overexpression reverses the effects of ZFAS1 knockdown on imatinib sensitivity and glucose metabolism reprogramming in IM-resistant K562 cells, including si-NC+NC, si-ZFAS1+NC, and si-ZFAS1+STAT3 IM-R K562 cells. (A) Drug sensitivity assay by CCK-8 showing relative cell viability of cells treated with varying concentrations of IM. (B) IC50 values were determined via CCK-8 assay after 48 hours of imatinib treatment. (C) Relative glucose uptake levels. (D) Relative lactate production. (E) Relative ATP levels. (F) ECAR over time. (G) Glycolysis and glycolytic capacity. (H) OCR over time. (I) Summary of basal respiration and maximal respiration. ** p <0.01, *** p <0.001 vs . si-NC+NC; # p <0.05, ## p <0.01, ### p <0.001 vs . si-ZFAS1+NC.

    Techniques Used: Over Expression, Knockdown, Sensitive Assay, CCK-8 Assay

    ZFAS1 promotes HIF1α upregulation through STAT3 in IM-resistant K562 cells. (A) Relative expression of STAT3 in IM-R K562 cells transfected with STAT3 plasmid compared to negative control (NC). (B) Western blot analysis showing the protein expression levels of HIF1α, LDHA, and PDK1 in si-NC, si-ZFAS1, and si-ZFAS1 + STAT3 transfected IM-R K562 cells. Data are presented as mean ± SD. *** p <0.001 vs . NC.
    Figure Legend Snippet: ZFAS1 promotes HIF1α upregulation through STAT3 in IM-resistant K562 cells. (A) Relative expression of STAT3 in IM-R K562 cells transfected with STAT3 plasmid compared to negative control (NC). (B) Western blot analysis showing the protein expression levels of HIF1α, LDHA, and PDK1 in si-NC, si-ZFAS1, and si-ZFAS1 + STAT3 transfected IM-R K562 cells. Data are presented as mean ± SD. *** p <0.001 vs . NC.

    Techniques Used: Expressing, Transfection, Plasmid Preparation, Negative Control, Western Blot

    Effect of 2-DG on STAT3 -mediated imatinib resistance in IM-R K562 cells. (A) CCK-8 assay shows relative cell viability of IM-R K562 cells with negative control (NC), STAT3 overexpression ( STAT3 ), and STAT3 treated with 2-DG ( STAT3 + 2-DG) under varying concentrations of imatinib. (B) IC50 values were determined via CCK-8 assay after 48 hours of imatinib treatment. ** p <0.01 vs . NC; # p <0.05 vs . STAT3.
    Figure Legend Snippet: Effect of 2-DG on STAT3 -mediated imatinib resistance in IM-R K562 cells. (A) CCK-8 assay shows relative cell viability of IM-R K562 cells with negative control (NC), STAT3 overexpression ( STAT3 ), and STAT3 treated with 2-DG ( STAT3 + 2-DG) under varying concentrations of imatinib. (B) IC50 values were determined via CCK-8 assay after 48 hours of imatinib treatment. ** p <0.01 vs . NC; # p <0.05 vs . STAT3.

    Techniques Used: CCK-8 Assay, Negative Control, Over Expression



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    Phase contrast images showing primary cultures of the human Wharton’s jelly stem cells (hWJSCs) derived from the umbilical cord obtained following normal full-term delivery at (A) early passage (P0) and (B) later passage (P5). (C) Phase contrast image of the human chronic myeloid leukemia cell line <t>(K562)</t> in culutre. (D) Representative histogram of the CD surface markers on the hWJSCs using fluorescent activated cell sorting (FACS) analysis. The MSC positive surface CD markers, namely, CD29, CD73, CD44, CD90, and CD105, and the MSC negative surface CD markers, namely, CD34 and CD45, are shown. The independent CD marker antigens were tagged with different fluorochromes. All the MSC positive CD surface markers demonstrated more than 90% positivity. PE, phycoerythrin; APC, allophycocyanin; FITC, fluorescein isothiocyanate.
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    Elevated expression of lncRNA ZFAS1 and STAT3 in imatinib-resistant (IM-R) CML patient samples and IM-R K562 cell line. (A, B) Relative expressions of ZFAS1 and STAT3 in peripheral blood cells from imatinib-resistant (IM-R, n=30) and imatinib-sensitive (IM-S, n=30) CML patients. (C) Correlation analysis between ZFAS1 and STAT3 in CML patients samples. (D, E) Expression levels of lncRNA ZFAS1 and STAT3 in IM-R and IM-S K562 cells. Data are presented as mean ± SD. *** p <0.001 vs . IM-S.

    Journal: Frontiers in Oncology

    Article Title: ZFAS1/STAT3 axis modulates imatinib resistance of chronic myeloid leukemia cells through glucose metabolism reprogramming

    doi: 10.3389/fonc.2025.1603060

    Figure Lengend Snippet: Elevated expression of lncRNA ZFAS1 and STAT3 in imatinib-resistant (IM-R) CML patient samples and IM-R K562 cell line. (A, B) Relative expressions of ZFAS1 and STAT3 in peripheral blood cells from imatinib-resistant (IM-R, n=30) and imatinib-sensitive (IM-S, n=30) CML patients. (C) Correlation analysis between ZFAS1 and STAT3 in CML patients samples. (D, E) Expression levels of lncRNA ZFAS1 and STAT3 in IM-R and IM-S K562 cells. Data are presented as mean ± SD. *** p <0.001 vs . IM-S.

    Article Snippet: Human leukemic cell line K562 cells were procured from ATCC in Manassas, VA, USA, and maintained in RMPI 1640 medium supplemented with 10% heat-inactivated FBS, 100 U/ml penicillin, and 100 μg/ml streptomycin.

    Techniques: Expressing

    Effects of ZFAS1 knockdown on imatinib-resistant K562 cells. (A) PCR analysis showing the efficiency of ZFAS1 knockdown in IM-R K562 cells. (B) Drug sensitivity assay (CCK-8) showing relative cell viability of si-NC and si-ZFAS1 IM-R K562 cells treated with varying concentrations of IM. (C) IC 50 values of imatinib in si-ZFAS1 cells and si-NC cells. (D) Colony formation assay showing the number of colonies formed by si-NC and si-ZFAS1 IM-R K562 cells treated with or without 2 µM IM. (E) Flow cytometry analysis showing the apoptosis rate of si-NC and si-ZFAS1 IM-R K562 cells treated with 2 µM IM. Data are presented as mean ± SD. NTC: non-treated control; ** p <0.01, *** p <0.001 vs . si-NC; ### p <0.001 vs . IM+si-NC.

    Journal: Frontiers in Oncology

    Article Title: ZFAS1/STAT3 axis modulates imatinib resistance of chronic myeloid leukemia cells through glucose metabolism reprogramming

    doi: 10.3389/fonc.2025.1603060

    Figure Lengend Snippet: Effects of ZFAS1 knockdown on imatinib-resistant K562 cells. (A) PCR analysis showing the efficiency of ZFAS1 knockdown in IM-R K562 cells. (B) Drug sensitivity assay (CCK-8) showing relative cell viability of si-NC and si-ZFAS1 IM-R K562 cells treated with varying concentrations of IM. (C) IC 50 values of imatinib in si-ZFAS1 cells and si-NC cells. (D) Colony formation assay showing the number of colonies formed by si-NC and si-ZFAS1 IM-R K562 cells treated with or without 2 µM IM. (E) Flow cytometry analysis showing the apoptosis rate of si-NC and si-ZFAS1 IM-R K562 cells treated with 2 µM IM. Data are presented as mean ± SD. NTC: non-treated control; ** p <0.01, *** p <0.001 vs . si-NC; ### p <0.001 vs . IM+si-NC.

    Article Snippet: Human leukemic cell line K562 cells were procured from ATCC in Manassas, VA, USA, and maintained in RMPI 1640 medium supplemented with 10% heat-inactivated FBS, 100 U/ml penicillin, and 100 μg/ml streptomycin.

    Techniques: Knockdown, Sensitive Assay, CCK-8 Assay, Colony Assay, Flow Cytometry, Control

    Effects of ZFAS1 knockdown on glucose metabolism in IM-R K562 cells. (A) Relative glucose uptake levels in si-NC and si-ZFAS1 IM-R K562 cells. (B) Relative lactate production in si-NC and si-ZFAS1 IM-R K562 cells. (C) Relative ATP levels in si-NC and si-ZFAS1 IM-R K562 cells. (D) Extracellular acidification rate (ECAR) in si-NC and si-ZFAS1 IM-R K562 cells. (E) Oxygen consumption rate (OCR) in si-NC and si-ZFAS1 IM-R K562 cells. (F) ECAR vs . OCR plot illustrating the metabolic shift in si-ZFAS1 IM-R K562 cells. (G) Comprehensive metabolic profile showing the impact of ZFAS1 knockdown on IM-R K562 cell metabolism. Data are presented as mean ± SD. ** p <0.01, *** p <0.001 vs . si-NC.

    Journal: Frontiers in Oncology

    Article Title: ZFAS1/STAT3 axis modulates imatinib resistance of chronic myeloid leukemia cells through glucose metabolism reprogramming

    doi: 10.3389/fonc.2025.1603060

    Figure Lengend Snippet: Effects of ZFAS1 knockdown on glucose metabolism in IM-R K562 cells. (A) Relative glucose uptake levels in si-NC and si-ZFAS1 IM-R K562 cells. (B) Relative lactate production in si-NC and si-ZFAS1 IM-R K562 cells. (C) Relative ATP levels in si-NC and si-ZFAS1 IM-R K562 cells. (D) Extracellular acidification rate (ECAR) in si-NC and si-ZFAS1 IM-R K562 cells. (E) Oxygen consumption rate (OCR) in si-NC and si-ZFAS1 IM-R K562 cells. (F) ECAR vs . OCR plot illustrating the metabolic shift in si-ZFAS1 IM-R K562 cells. (G) Comprehensive metabolic profile showing the impact of ZFAS1 knockdown on IM-R K562 cell metabolism. Data are presented as mean ± SD. ** p <0.01, *** p <0.001 vs . si-NC.

    Article Snippet: Human leukemic cell line K562 cells were procured from ATCC in Manassas, VA, USA, and maintained in RMPI 1640 medium supplemented with 10% heat-inactivated FBS, 100 U/ml penicillin, and 100 μg/ml streptomycin.

    Techniques: Knockdown

    STAT3 overexpression reverses the effects of ZFAS1 knockdown on imatinib sensitivity and glucose metabolism reprogramming in IM-resistant K562 cells, including si-NC+NC, si-ZFAS1+NC, and si-ZFAS1+STAT3 IM-R K562 cells. (A) Drug sensitivity assay by CCK-8 showing relative cell viability of cells treated with varying concentrations of IM. (B) IC50 values were determined via CCK-8 assay after 48 hours of imatinib treatment. (C) Relative glucose uptake levels. (D) Relative lactate production. (E) Relative ATP levels. (F) ECAR over time. (G) Glycolysis and glycolytic capacity. (H) OCR over time. (I) Summary of basal respiration and maximal respiration. ** p <0.01, *** p <0.001 vs . si-NC+NC; # p <0.05, ## p <0.01, ### p <0.001 vs . si-ZFAS1+NC.

    Journal: Frontiers in Oncology

    Article Title: ZFAS1/STAT3 axis modulates imatinib resistance of chronic myeloid leukemia cells through glucose metabolism reprogramming

    doi: 10.3389/fonc.2025.1603060

    Figure Lengend Snippet: STAT3 overexpression reverses the effects of ZFAS1 knockdown on imatinib sensitivity and glucose metabolism reprogramming in IM-resistant K562 cells, including si-NC+NC, si-ZFAS1+NC, and si-ZFAS1+STAT3 IM-R K562 cells. (A) Drug sensitivity assay by CCK-8 showing relative cell viability of cells treated with varying concentrations of IM. (B) IC50 values were determined via CCK-8 assay after 48 hours of imatinib treatment. (C) Relative glucose uptake levels. (D) Relative lactate production. (E) Relative ATP levels. (F) ECAR over time. (G) Glycolysis and glycolytic capacity. (H) OCR over time. (I) Summary of basal respiration and maximal respiration. ** p <0.01, *** p <0.001 vs . si-NC+NC; # p <0.05, ## p <0.01, ### p <0.001 vs . si-ZFAS1+NC.

    Article Snippet: Human leukemic cell line K562 cells were procured from ATCC in Manassas, VA, USA, and maintained in RMPI 1640 medium supplemented with 10% heat-inactivated FBS, 100 U/ml penicillin, and 100 μg/ml streptomycin.

    Techniques: Over Expression, Knockdown, Sensitive Assay, CCK-8 Assay

    ZFAS1 promotes HIF1α upregulation through STAT3 in IM-resistant K562 cells. (A) Relative expression of STAT3 in IM-R K562 cells transfected with STAT3 plasmid compared to negative control (NC). (B) Western blot analysis showing the protein expression levels of HIF1α, LDHA, and PDK1 in si-NC, si-ZFAS1, and si-ZFAS1 + STAT3 transfected IM-R K562 cells. Data are presented as mean ± SD. *** p <0.001 vs . NC.

    Journal: Frontiers in Oncology

    Article Title: ZFAS1/STAT3 axis modulates imatinib resistance of chronic myeloid leukemia cells through glucose metabolism reprogramming

    doi: 10.3389/fonc.2025.1603060

    Figure Lengend Snippet: ZFAS1 promotes HIF1α upregulation through STAT3 in IM-resistant K562 cells. (A) Relative expression of STAT3 in IM-R K562 cells transfected with STAT3 plasmid compared to negative control (NC). (B) Western blot analysis showing the protein expression levels of HIF1α, LDHA, and PDK1 in si-NC, si-ZFAS1, and si-ZFAS1 + STAT3 transfected IM-R K562 cells. Data are presented as mean ± SD. *** p <0.001 vs . NC.

    Article Snippet: Human leukemic cell line K562 cells were procured from ATCC in Manassas, VA, USA, and maintained in RMPI 1640 medium supplemented with 10% heat-inactivated FBS, 100 U/ml penicillin, and 100 μg/ml streptomycin.

    Techniques: Expressing, Transfection, Plasmid Preparation, Negative Control, Western Blot

    Effect of 2-DG on STAT3 -mediated imatinib resistance in IM-R K562 cells. (A) CCK-8 assay shows relative cell viability of IM-R K562 cells with negative control (NC), STAT3 overexpression ( STAT3 ), and STAT3 treated with 2-DG ( STAT3 + 2-DG) under varying concentrations of imatinib. (B) IC50 values were determined via CCK-8 assay after 48 hours of imatinib treatment. ** p <0.01 vs . NC; # p <0.05 vs . STAT3.

    Journal: Frontiers in Oncology

    Article Title: ZFAS1/STAT3 axis modulates imatinib resistance of chronic myeloid leukemia cells through glucose metabolism reprogramming

    doi: 10.3389/fonc.2025.1603060

    Figure Lengend Snippet: Effect of 2-DG on STAT3 -mediated imatinib resistance in IM-R K562 cells. (A) CCK-8 assay shows relative cell viability of IM-R K562 cells with negative control (NC), STAT3 overexpression ( STAT3 ), and STAT3 treated with 2-DG ( STAT3 + 2-DG) under varying concentrations of imatinib. (B) IC50 values were determined via CCK-8 assay after 48 hours of imatinib treatment. ** p <0.01 vs . NC; # p <0.05 vs . STAT3.

    Article Snippet: Human leukemic cell line K562 cells were procured from ATCC in Manassas, VA, USA, and maintained in RMPI 1640 medium supplemented with 10% heat-inactivated FBS, 100 U/ml penicillin, and 100 μg/ml streptomycin.

    Techniques: CCK-8 Assay, Negative Control, Over Expression

    The time- and concentration-dependent effects of Fdb on ( A ) LLC-MK2 and ( B ) K562 cells. The cultured cells were treated with Fdb concentrations of 0, 2.5, 5, and 10 µM. Percentage of cell viability was determined after 24, 72, and 96 h of incubation at 37 °C in a 5% CO 2 incubator by MTT assay. The dotted line indicates axis intercepts of IC 50 and the log (dose) estimating value.

    Journal: Medical Sciences

    Article Title: Combined Effects of Fludarabine and Interferon Alpha on Autophagy Regulation Define the Phase of Cell Survival and Promotes Responses in LLC-MK2 and K562 Cells

    doi: 10.3390/medsci10010020

    Figure Lengend Snippet: The time- and concentration-dependent effects of Fdb on ( A ) LLC-MK2 and ( B ) K562 cells. The cultured cells were treated with Fdb concentrations of 0, 2.5, 5, and 10 µM. Percentage of cell viability was determined after 24, 72, and 96 h of incubation at 37 °C in a 5% CO 2 incubator by MTT assay. The dotted line indicates axis intercepts of IC 50 and the log (dose) estimating value.

    Article Snippet: LLC-MK2, the rhesus monkey kidney epithelial cell line, and the K562 human leukemic cell line were purchased from ATCC (Manassas, VA, USA), propagated, and stocked at −80 °C.

    Techniques: Concentration Assay, Cell Culture, Incubation, MTT Assay

    Western blot analysis of protein expression in LLC-MK2 and K562 cell treatment with Fdb (concentrations 0, 2.5, 5, 10 µM) for 24 h. The total cellular proteins were extracted and transferred to nitrocellulose membranes. The membranes were immunostained with specific antibodies against the autophagy-related proteins p-mTOR, Beclin-1, and LC3B-I/LC3B-II and processed for reaction color development. β-Actin was used as an internal control.

    Journal: Medical Sciences

    Article Title: Combined Effects of Fludarabine and Interferon Alpha on Autophagy Regulation Define the Phase of Cell Survival and Promotes Responses in LLC-MK2 and K562 Cells

    doi: 10.3390/medsci10010020

    Figure Lengend Snippet: Western blot analysis of protein expression in LLC-MK2 and K562 cell treatment with Fdb (concentrations 0, 2.5, 5, 10 µM) for 24 h. The total cellular proteins were extracted and transferred to nitrocellulose membranes. The membranes were immunostained with specific antibodies against the autophagy-related proteins p-mTOR, Beclin-1, and LC3B-I/LC3B-II and processed for reaction color development. β-Actin was used as an internal control.

    Article Snippet: LLC-MK2, the rhesus monkey kidney epithelial cell line, and the K562 human leukemic cell line were purchased from ATCC (Manassas, VA, USA), propagated, and stocked at −80 °C.

    Techniques: Western Blot, Expressing, Control

    Western blot analysis of autophagy response and the antiviral response in cultured LLC-MK2 and K562 cells that were exposed for 60 min to IFN-α (10 U/mL) before treatment with Fdb (10 μM) for 24 h. The cells were evaluated for autophagy response mediation via p-mTOR and LC3B-I/LC3B-II activation, as well as antiviral response via p-STAT1 signaling molecules. The total proteins were extracted and transferred to nitrocellulose membranes. The membranes were immunostained with p-mTOR, LC3B-I/LC3B-II, and p-STAT1 antibodies and processed for reaction color development. β-Actin was used as an internal control. Protein electrophoresis films were digitized and the relative density level of p-mTOR (normalized with β-Actin), autophagosome marker LC3B-II (normalized with LC3B-I), and p-STAT1 (normalized with β-Actin) were measured by using ImageJ ® software. One-way ANOVA statistical analysis was performed (*, **, *** indicates a p -value of <0.05, 0.01, 0.001, respectively). The experiments were analyzed in triplicate and SEM is marked by an error bar.

    Journal: Medical Sciences

    Article Title: Combined Effects of Fludarabine and Interferon Alpha on Autophagy Regulation Define the Phase of Cell Survival and Promotes Responses in LLC-MK2 and K562 Cells

    doi: 10.3390/medsci10010020

    Figure Lengend Snippet: Western blot analysis of autophagy response and the antiviral response in cultured LLC-MK2 and K562 cells that were exposed for 60 min to IFN-α (10 U/mL) before treatment with Fdb (10 μM) for 24 h. The cells were evaluated for autophagy response mediation via p-mTOR and LC3B-I/LC3B-II activation, as well as antiviral response via p-STAT1 signaling molecules. The total proteins were extracted and transferred to nitrocellulose membranes. The membranes were immunostained with p-mTOR, LC3B-I/LC3B-II, and p-STAT1 antibodies and processed for reaction color development. β-Actin was used as an internal control. Protein electrophoresis films were digitized and the relative density level of p-mTOR (normalized with β-Actin), autophagosome marker LC3B-II (normalized with LC3B-I), and p-STAT1 (normalized with β-Actin) were measured by using ImageJ ® software. One-way ANOVA statistical analysis was performed (*, **, *** indicates a p -value of <0.05, 0.01, 0.001, respectively). The experiments were analyzed in triplicate and SEM is marked by an error bar.

    Article Snippet: LLC-MK2, the rhesus monkey kidney epithelial cell line, and the K562 human leukemic cell line were purchased from ATCC (Manassas, VA, USA), propagated, and stocked at −80 °C.

    Techniques: Western Blot, Cell Culture, Activation Assay, Control, Protein Electrophoresis, Marker, Software

    Phase contrast images showing primary cultures of the human Wharton’s jelly stem cells (hWJSCs) derived from the umbilical cord obtained following normal full-term delivery at (A) early passage (P0) and (B) later passage (P5). (C) Phase contrast image of the human chronic myeloid leukemia cell line (K562) in culutre. (D) Representative histogram of the CD surface markers on the hWJSCs using fluorescent activated cell sorting (FACS) analysis. The MSC positive surface CD markers, namely, CD29, CD73, CD44, CD90, and CD105, and the MSC negative surface CD markers, namely, CD34 and CD45, are shown. The independent CD marker antigens were tagged with different fluorochromes. All the MSC positive CD surface markers demonstrated more than 90% positivity. PE, phycoerythrin; APC, allophycocyanin; FITC, fluorescein isothiocyanate.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Human Wharton’s Jelly Stem Cell Secretions Inhibit Human Leukemic Cell Line K562 in vitro by Inducing Cell Cycle Arrest and Apoptosis

    doi: 10.3389/fcell.2021.614988

    Figure Lengend Snippet: Phase contrast images showing primary cultures of the human Wharton’s jelly stem cells (hWJSCs) derived from the umbilical cord obtained following normal full-term delivery at (A) early passage (P0) and (B) later passage (P5). (C) Phase contrast image of the human chronic myeloid leukemia cell line (K562) in culutre. (D) Representative histogram of the CD surface markers on the hWJSCs using fluorescent activated cell sorting (FACS) analysis. The MSC positive surface CD markers, namely, CD29, CD73, CD44, CD90, and CD105, and the MSC negative surface CD markers, namely, CD34 and CD45, are shown. The independent CD marker antigens were tagged with different fluorochromes. All the MSC positive CD surface markers demonstrated more than 90% positivity. PE, phycoerythrin; APC, allophycocyanin; FITC, fluorescein isothiocyanate.

    Article Snippet: The commercial human leukemic cell line (K562) was purchased from the American Type Culture Collection (ATCC, MD, United States).

    Techniques: Derivative Assay, FACS, Marker

    (A) In vitro differentiation images of the human Wharton’s jelly stem cells (hWJSCs) into adipocytes (top row), chondrocytes (middle row), and osteocytes (bottom row). The left column represents the respective controls, the middle column shows the differentiated images, and the right column is the magnified images of the boxed area. (B) Phase contrast images of the chronic myeloid leukemai cell line (K562) treated with the hWJSC co-culture (hWJSC-CC, top row), hWJSC-conditioned medium [hWJSC-CM (100%), middle row), and hWJSC lysate (hWJSC-L (15 μg/ml), bottom row] for 24, 48, and 72 h. A mild to moderate decrease in the K562 cells was eveident with an increase in cell death (black arrows) with time following treatment with the hWJSCs or their extracts.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Human Wharton’s Jelly Stem Cell Secretions Inhibit Human Leukemic Cell Line K562 in vitro by Inducing Cell Cycle Arrest and Apoptosis

    doi: 10.3389/fcell.2021.614988

    Figure Lengend Snippet: (A) In vitro differentiation images of the human Wharton’s jelly stem cells (hWJSCs) into adipocytes (top row), chondrocytes (middle row), and osteocytes (bottom row). The left column represents the respective controls, the middle column shows the differentiated images, and the right column is the magnified images of the boxed area. (B) Phase contrast images of the chronic myeloid leukemai cell line (K562) treated with the hWJSC co-culture (hWJSC-CC, top row), hWJSC-conditioned medium [hWJSC-CM (100%), middle row), and hWJSC lysate (hWJSC-L (15 μg/ml), bottom row] for 24, 48, and 72 h. A mild to moderate decrease in the K562 cells was eveident with an increase in cell death (black arrows) with time following treatment with the hWJSCs or their extracts.

    Article Snippet: The commercial human leukemic cell line (K562) was purchased from the American Type Culture Collection (ATCC, MD, United States).

    Techniques: In Vitro, Co-Culture Assay

    Cell metabolic activity (MTT) assay showing the cell growth profiles of (A) the human Wharton’s jelly stem cells (hWJSCs), (B) the chronic myeloid leukemai cell line (K562), and (C) the K562 cells treated with the hWJSC co-culture (hWJSC-CC), hWJSC-conditioned medium (hWJSC-CM, 100%), and hWJSC lysate (hWJSC-L, 15 μg/ml) for 24, 48, and 72 h. Mean increases in proliferation of the hWJSCs and K562 cells indicative of their biological cell growth characteristics were observed (A,B) . Mean decreases in proliferation of the K562 cells were observed following treatment with the hWJSCs and their extracts (hWJSC-CM, hWJSC-L) especially at 48 and 72 h, and these decreases were statistically significant compared with the control (C) . The values are expressed as mean ± SEM of three different experiments. ∗ indicates statistical significance ( P < 0.05).

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Human Wharton’s Jelly Stem Cell Secretions Inhibit Human Leukemic Cell Line K562 in vitro by Inducing Cell Cycle Arrest and Apoptosis

    doi: 10.3389/fcell.2021.614988

    Figure Lengend Snippet: Cell metabolic activity (MTT) assay showing the cell growth profiles of (A) the human Wharton’s jelly stem cells (hWJSCs), (B) the chronic myeloid leukemai cell line (K562), and (C) the K562 cells treated with the hWJSC co-culture (hWJSC-CC), hWJSC-conditioned medium (hWJSC-CM, 100%), and hWJSC lysate (hWJSC-L, 15 μg/ml) for 24, 48, and 72 h. Mean increases in proliferation of the hWJSCs and K562 cells indicative of their biological cell growth characteristics were observed (A,B) . Mean decreases in proliferation of the K562 cells were observed following treatment with the hWJSCs and their extracts (hWJSC-CM, hWJSC-L) especially at 48 and 72 h, and these decreases were statistically significant compared with the control (C) . The values are expressed as mean ± SEM of three different experiments. ∗ indicates statistical significance ( P < 0.05).

    Article Snippet: The commercial human leukemic cell line (K562) was purchased from the American Type Culture Collection (ATCC, MD, United States).

    Techniques: Activity Assay, MTT Assay, Co-Culture Assay, Control

    (A) Cell cycle (propidium iodide) assay. The K562 cells treated with the hWJSC co-culture (hWJSC-CC), hWJSC-conditioned medium (hWJSC-CM, 100%), and hWJSC lysate (hWJSC-L, 15 μg/ml) for 48 h showed an increase in the G2M phase of the cell cycle indicative of metaphase arrest. (B) Annexin V–APC and PI assay. The K562 cells treated as above with the hWJSCs and hWJSC extracts for 48 h showed an increase in the number of apoptosis cells compared with the control.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Human Wharton’s Jelly Stem Cell Secretions Inhibit Human Leukemic Cell Line K562 in vitro by Inducing Cell Cycle Arrest and Apoptosis

    doi: 10.3389/fcell.2021.614988

    Figure Lengend Snippet: (A) Cell cycle (propidium iodide) assay. The K562 cells treated with the hWJSC co-culture (hWJSC-CC), hWJSC-conditioned medium (hWJSC-CM, 100%), and hWJSC lysate (hWJSC-L, 15 μg/ml) for 48 h showed an increase in the G2M phase of the cell cycle indicative of metaphase arrest. (B) Annexin V–APC and PI assay. The K562 cells treated as above with the hWJSCs and hWJSC extracts for 48 h showed an increase in the number of apoptosis cells compared with the control.

    Article Snippet: The commercial human leukemic cell line (K562) was purchased from the American Type Culture Collection (ATCC, MD, United States).

    Techniques: Co-Culture Assay, Control

    Expression levels of cytokines in the cell culture supernatant of the K562 cells treated with the hWJSC co-culture (hWJSC-CC), hWJSC-conditioned medium (hWJSC-CM, 100%), and hWJSC lysate (hWJSC-L, 15 μg/ml) for 48 h and analyzed using multiplex cytokine assay. The following pro-inflammation-related cytokines, namely, IFN-γ (A) , TNF-α (B) , IL-1β (C) , IL-6 (D) , IL-8 (E) , and IL-12 (F) , were decreased compared with the control. The anti-inflammatory cytokine IL-10 (G) was increased compared with the control. The values are expressed as mean ± SEM of three different experiments. ∗ indicates statistical significance ( P < 0.05) compared with the control.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Human Wharton’s Jelly Stem Cell Secretions Inhibit Human Leukemic Cell Line K562 in vitro by Inducing Cell Cycle Arrest and Apoptosis

    doi: 10.3389/fcell.2021.614988

    Figure Lengend Snippet: Expression levels of cytokines in the cell culture supernatant of the K562 cells treated with the hWJSC co-culture (hWJSC-CC), hWJSC-conditioned medium (hWJSC-CM, 100%), and hWJSC lysate (hWJSC-L, 15 μg/ml) for 48 h and analyzed using multiplex cytokine assay. The following pro-inflammation-related cytokines, namely, IFN-γ (A) , TNF-α (B) , IL-1β (C) , IL-6 (D) , IL-8 (E) , and IL-12 (F) , were decreased compared with the control. The anti-inflammatory cytokine IL-10 (G) was increased compared with the control. The values are expressed as mean ± SEM of three different experiments. ∗ indicates statistical significance ( P < 0.05) compared with the control.

    Article Snippet: The commercial human leukemic cell line (K562) was purchased from the American Type Culture Collection (ATCC, MD, United States).

    Techniques: Expressing, Cell Culture, Co-Culture Assay, Multiplex Assay, Cytokine Assay, Control