Journal: Hereditas

Article Title: MiR-143-5p serves as a diagnostic biomarker in patients with sepsis and regulates sepsis-induced inflammation and cardiac dysfunction

doi: 10.1186/s41065-025-00623-0

Figure Lengend Snippet: The effect of miR-143-5p on LPS-induced THP-1. a The miR-143-5p expression was downregulated in LPS-induced THP-1 and could be upregulated by miR-143-5p mimic transfection. b - c Overexpression of miR-143-5p suppressed the level of ( b ) M1 polarization markers (iNOS and CD86) and improved the ( c ) M2 polarization markers (Arg-1 and CD206) expression in LPS-induced THP-1. d MiR-143-5p upregulation inhibited the level of inflammatory cytokines, including TNF-α and IL-6, in THP-1 induced by LPS. ns: no significance, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Statistical tests: one-way ANOVA with post hoc Tukey’s test

Article Snippet: Human leukemic monocytic cell line THP-1 (ATCC, USA).

Techniques: Expressing, Transfection, Over Expression

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

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

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

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

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

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