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mhcc 97h hepg2  (ATCC)


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    ATCC mhcc 97h hepg2
    Expression of HOTAIR was upregulated in liver cancer tissues and liver cancer cell lines. (A) The expression of HOTAIR in tumor tissues and normal tissues was detected by qRT-RCR. (B) The expression of HOTAIR in 3 liver cancer cell lines (MHCC <t>97H,</t> <t>HepG2</t> and <t>Hep3B)</t> and normal human hepatic cell line HL-7702 was evaluated by qRT-RCR. (C) The expression of HOTAIR in tumor tissues and normal tissues was measured by northern blotting. (D) The expression of HOTAIR in MHCC 97H, HepG2, Hep3B and HL-7702 cell lines was measured by northern blotting (*P<0.05, **P<0.01). HOTAIR, HOX transcript antisense RNA
    Mhcc 97h Hepg2, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 29754 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mhcc+97h+hepg2/Hep+G2/pmc05962869-157-12-20
    Average 99 stars, based on 29754 article reviews
    mhcc 97h hepg2 - by Bioz Stars, 2026-08
    99/100 stars

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    1) Product Images from "HOTAIR contributes to the growth of liver cancer via targeting miR-217"

    Article Title: HOTAIR contributes to the growth of liver cancer via targeting miR-217

    Journal: Oncology Letters

    doi: 10.3892/ol.2018.8341

    Expression of HOTAIR was upregulated in liver cancer tissues and liver cancer cell lines. (A) The expression of HOTAIR in tumor tissues and normal tissues was detected by qRT-RCR. (B) The expression of HOTAIR in 3 liver cancer cell lines (MHCC 97H, HepG2 and Hep3B) and normal human hepatic cell line HL-7702 was evaluated by qRT-RCR. (C) The expression of HOTAIR in tumor tissues and normal tissues was measured by northern blotting. (D) The expression of HOTAIR in MHCC 97H, HepG2, Hep3B and HL-7702 cell lines was measured by northern blotting (*P<0.05, **P<0.01). HOTAIR, HOX transcript antisense RNA
    Figure Legend Snippet: Expression of HOTAIR was upregulated in liver cancer tissues and liver cancer cell lines. (A) The expression of HOTAIR in tumor tissues and normal tissues was detected by qRT-RCR. (B) The expression of HOTAIR in 3 liver cancer cell lines (MHCC 97H, HepG2 and Hep3B) and normal human hepatic cell line HL-7702 was evaluated by qRT-RCR. (C) The expression of HOTAIR in tumor tissues and normal tissues was measured by northern blotting. (D) The expression of HOTAIR in MHCC 97H, HepG2, Hep3B and HL-7702 cell lines was measured by northern blotting (*P<0.05, **P<0.01). HOTAIR, HOX transcript antisense RNA

    Techniques Used: Expressing, Northern Blot

    HOTAIR inhibition suppressed the proliferation of HepG2 cells. HepG2 cells were infected with HOTAIR siRNA lentiviral vectors or the empty lentiviral vectors for 72 h. (A) The expression of HOTAIR was evaluated by qRT-RCR. (B) The proliferation rate was measured by CCK-8 assay. (C and D) The cell number was assessed by optical microscope. (E) The protein expression of two proliferation marker proteins Ki67 and PCNA was evaluated by western blotting. GAPDH was used as an internal control (*P<0.05, ***P<0.001). HOTAIR, HOX transcript antisense RNA.
    Figure Legend Snippet: HOTAIR inhibition suppressed the proliferation of HepG2 cells. HepG2 cells were infected with HOTAIR siRNA lentiviral vectors or the empty lentiviral vectors for 72 h. (A) The expression of HOTAIR was evaluated by qRT-RCR. (B) The proliferation rate was measured by CCK-8 assay. (C and D) The cell number was assessed by optical microscope. (E) The protein expression of two proliferation marker proteins Ki67 and PCNA was evaluated by western blotting. GAPDH was used as an internal control (*P<0.05, ***P<0.001). HOTAIR, HOX transcript antisense RNA.

    Techniques Used: Inhibition, Infection, Expressing, CCK-8 Assay, Microscopy, Marker, Western Blot

    HOTAIR directly targeted miR-217. (A) HepG2 cells were transfected with miR-217 mimics or miR-217 mock alone, or co-transfected with HOTAIR siRNA lentiviral vectors together. The expression of miR-217 was evaluated by northern blotting. (B) HepG2 cells were transfected with miR-217 inhibitors or miR-217 mock alone, or co-transfected with HOTAIR siRNA lentiviral vectors together. The expression of miR-217 was evaluated by northern blotting. (C) HepG2 cells were co-transfected with pGL3 plasmids containing HOTAIR (WT or MUT) sequences and miR-217 mimics. The luciferase activity was detected by luciferase reporter assay. (D) The expression correlation between HOTAIR and mir-217 was determined in 25 liver cancer tissues (**P<0.01). HOTAIR, HOX transcript antisense RNA. miR-217, microRNA-217.
    Figure Legend Snippet: HOTAIR directly targeted miR-217. (A) HepG2 cells were transfected with miR-217 mimics or miR-217 mock alone, or co-transfected with HOTAIR siRNA lentiviral vectors together. The expression of miR-217 was evaluated by northern blotting. (B) HepG2 cells were transfected with miR-217 inhibitors or miR-217 mock alone, or co-transfected with HOTAIR siRNA lentiviral vectors together. The expression of miR-217 was evaluated by northern blotting. (C) HepG2 cells were co-transfected with pGL3 plasmids containing HOTAIR (WT or MUT) sequences and miR-217 mimics. The luciferase activity was detected by luciferase reporter assay. (D) The expression correlation between HOTAIR and mir-217 was determined in 25 liver cancer tissues (**P<0.01). HOTAIR, HOX transcript antisense RNA. miR-217, microRNA-217.

    Techniques Used: Transfection, Expressing, Northern Blot, Luciferase, Activity Assay, Reporter Assay

    miR-217 was involved in the regulation of HOTAIR on cell proliferation and cycle arrest in HepG2 cells. HepG2 cells were transfected with HOTAIR siRNA lentiviral vectors or miR-217 inhibitors, or the combination. (A) The proliferation rate was measured by CCK-8 assay. (B) The cell number was assessed by optical microscope. (C) The protein expression of Ki67, PCNA, p27 and cyclin D1 was evaluated by western blotting. (D) The cell cycle arrest was evaluated by flow cytometry (**P<0.01). HOTAIR, HOX transcript antisense RNA. miR-217, microRNA-217.
    Figure Legend Snippet: miR-217 was involved in the regulation of HOTAIR on cell proliferation and cycle arrest in HepG2 cells. HepG2 cells were transfected with HOTAIR siRNA lentiviral vectors or miR-217 inhibitors, or the combination. (A) The proliferation rate was measured by CCK-8 assay. (B) The cell number was assessed by optical microscope. (C) The protein expression of Ki67, PCNA, p27 and cyclin D1 was evaluated by western blotting. (D) The cell cycle arrest was evaluated by flow cytometry (**P<0.01). HOTAIR, HOX transcript antisense RNA. miR-217, microRNA-217.

    Techniques Used: Transfection, CCK-8 Assay, Microscopy, Expressing, Western Blot, Flow Cytometry

    HOTAIR inhibition suppresses tumor growth in xenograft models. Xenograft mouse model was created by subcutaneous injection of HepG2 cells pretreated with or without HOTAIR siRNA lentiviral vectors to nude mouse. (A) Five primary tumors from each group were photographed after sacrifice at 30th day. (B) Tumor growth curves in two groups were shown every 6 days until the 30th day following cells injection. (C and D) The expression of HPTAIR and miR-217 in primary tumor tissues was measured by qRT-PCR. (E and F) The expression of HPTAIR and miR-217 in primary tumor tissues was measured by northern blotting. (G and H) The expression of Ki67 and PCNA in primary tumor tissues was visualized by immunohistochemistry (*P<0.05, **P<0.01). HOTAIR, HOX transcript antisense RNA. miR-217, microRNA-217.
    Figure Legend Snippet: HOTAIR inhibition suppresses tumor growth in xenograft models. Xenograft mouse model was created by subcutaneous injection of HepG2 cells pretreated with or without HOTAIR siRNA lentiviral vectors to nude mouse. (A) Five primary tumors from each group were photographed after sacrifice at 30th day. (B) Tumor growth curves in two groups were shown every 6 days until the 30th day following cells injection. (C and D) The expression of HPTAIR and miR-217 in primary tumor tissues was measured by qRT-PCR. (E and F) The expression of HPTAIR and miR-217 in primary tumor tissues was measured by northern blotting. (G and H) The expression of Ki67 and PCNA in primary tumor tissues was visualized by immunohistochemistry (*P<0.05, **P<0.01). HOTAIR, HOX transcript antisense RNA. miR-217, microRNA-217.

    Techniques Used: Inhibition, Injection, Expressing, Quantitative RT-PCR, Northern Blot, Immunohistochemistry



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    Expression of HOTAIR was upregulated in liver cancer tissues and liver cancer cell lines. (A) The expression of HOTAIR in tumor tissues and normal tissues was detected by qRT-RCR. (B) The expression of HOTAIR in 3 liver cancer cell lines (MHCC <t>97H,</t> <t>HepG2</t> and <t>Hep3B)</t> and normal human hepatic cell line HL-7702 was evaluated by qRT-RCR. (C) The expression of HOTAIR in tumor tissues and normal tissues was measured by northern blotting. (D) The expression of HOTAIR in MHCC 97H, HepG2, Hep3B and HL-7702 cell lines was measured by northern blotting (*P<0.05, **P<0.01). HOTAIR, HOX transcript antisense RNA
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    KRT19 binds a lincRNA Linc-KILH in <t>HCC</t> cells. (A) The expression level of KRT19 in HCC cell lines was detected by immunoblotting. (B) <t>Huh7</t> cells were subjected to RIP assays with a KRT19 antibody or isotype-matched control IgG, RIP-Seq analysis showing average-normalized, log2 transformed FPKM value of KRT19-RIP and input. (C) The amount of Linc-KILH in the precipitates was analyzed by quantitative real-time PCR analysis. RNA enrichment indicates the RNA levels of Linc-KILH or GAPDH in the anti-KRT19 precipitates relative to those in the IgG precipitates. D, Biotin-labeled Linc-KILH and Linc-KILH-AS were incubated with Huh7 cell lysate, and KRT19 interaction was confirmed by Western blotting. * P < 0.05.
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    Expression of HOTAIR was upregulated in liver cancer tissues and liver cancer cell lines. (A) The expression of HOTAIR in tumor tissues and normal tissues was detected by qRT-RCR. (B) The expression of HOTAIR in 3 liver cancer cell lines (MHCC 97H, HepG2 and Hep3B) and normal human hepatic cell line HL-7702 was evaluated by qRT-RCR. (C) The expression of HOTAIR in tumor tissues and normal tissues was measured by northern blotting. (D) The expression of HOTAIR in MHCC 97H, HepG2, Hep3B and HL-7702 cell lines was measured by northern blotting (*P<0.05, **P<0.01). HOTAIR, HOX transcript antisense RNA

    Journal: Oncology Letters

    Article Title: HOTAIR contributes to the growth of liver cancer via targeting miR-217

    doi: 10.3892/ol.2018.8341

    Figure Lengend Snippet: Expression of HOTAIR was upregulated in liver cancer tissues and liver cancer cell lines. (A) The expression of HOTAIR in tumor tissues and normal tissues was detected by qRT-RCR. (B) The expression of HOTAIR in 3 liver cancer cell lines (MHCC 97H, HepG2 and Hep3B) and normal human hepatic cell line HL-7702 was evaluated by qRT-RCR. (C) The expression of HOTAIR in tumor tissues and normal tissues was measured by northern blotting. (D) The expression of HOTAIR in MHCC 97H, HepG2, Hep3B and HL-7702 cell lines was measured by northern blotting (*P<0.05, **P<0.01). HOTAIR, HOX transcript antisense RNA

    Article Snippet: The normal human hepatic cell line HL-7702 and liver cancer cell lines (MHCC 97H, HepG2 and Hep3B) were obtained from American Type Culture Collection (Manassas, VA, USA).

    Techniques: Expressing, Northern Blot

    HOTAIR inhibition suppressed the proliferation of HepG2 cells. HepG2 cells were infected with HOTAIR siRNA lentiviral vectors or the empty lentiviral vectors for 72 h. (A) The expression of HOTAIR was evaluated by qRT-RCR. (B) The proliferation rate was measured by CCK-8 assay. (C and D) The cell number was assessed by optical microscope. (E) The protein expression of two proliferation marker proteins Ki67 and PCNA was evaluated by western blotting. GAPDH was used as an internal control (*P<0.05, ***P<0.001). HOTAIR, HOX transcript antisense RNA.

    Journal: Oncology Letters

    Article Title: HOTAIR contributes to the growth of liver cancer via targeting miR-217

    doi: 10.3892/ol.2018.8341

    Figure Lengend Snippet: HOTAIR inhibition suppressed the proliferation of HepG2 cells. HepG2 cells were infected with HOTAIR siRNA lentiviral vectors or the empty lentiviral vectors for 72 h. (A) The expression of HOTAIR was evaluated by qRT-RCR. (B) The proliferation rate was measured by CCK-8 assay. (C and D) The cell number was assessed by optical microscope. (E) The protein expression of two proliferation marker proteins Ki67 and PCNA was evaluated by western blotting. GAPDH was used as an internal control (*P<0.05, ***P<0.001). HOTAIR, HOX transcript antisense RNA.

    Article Snippet: The normal human hepatic cell line HL-7702 and liver cancer cell lines (MHCC 97H, HepG2 and Hep3B) were obtained from American Type Culture Collection (Manassas, VA, USA).

    Techniques: Inhibition, Infection, Expressing, CCK-8 Assay, Microscopy, Marker, Western Blot

    HOTAIR directly targeted miR-217. (A) HepG2 cells were transfected with miR-217 mimics or miR-217 mock alone, or co-transfected with HOTAIR siRNA lentiviral vectors together. The expression of miR-217 was evaluated by northern blotting. (B) HepG2 cells were transfected with miR-217 inhibitors or miR-217 mock alone, or co-transfected with HOTAIR siRNA lentiviral vectors together. The expression of miR-217 was evaluated by northern blotting. (C) HepG2 cells were co-transfected with pGL3 plasmids containing HOTAIR (WT or MUT) sequences and miR-217 mimics. The luciferase activity was detected by luciferase reporter assay. (D) The expression correlation between HOTAIR and mir-217 was determined in 25 liver cancer tissues (**P<0.01). HOTAIR, HOX transcript antisense RNA. miR-217, microRNA-217.

    Journal: Oncology Letters

    Article Title: HOTAIR contributes to the growth of liver cancer via targeting miR-217

    doi: 10.3892/ol.2018.8341

    Figure Lengend Snippet: HOTAIR directly targeted miR-217. (A) HepG2 cells were transfected with miR-217 mimics or miR-217 mock alone, or co-transfected with HOTAIR siRNA lentiviral vectors together. The expression of miR-217 was evaluated by northern blotting. (B) HepG2 cells were transfected with miR-217 inhibitors or miR-217 mock alone, or co-transfected with HOTAIR siRNA lentiviral vectors together. The expression of miR-217 was evaluated by northern blotting. (C) HepG2 cells were co-transfected with pGL3 plasmids containing HOTAIR (WT or MUT) sequences and miR-217 mimics. The luciferase activity was detected by luciferase reporter assay. (D) The expression correlation between HOTAIR and mir-217 was determined in 25 liver cancer tissues (**P<0.01). HOTAIR, HOX transcript antisense RNA. miR-217, microRNA-217.

    Article Snippet: The normal human hepatic cell line HL-7702 and liver cancer cell lines (MHCC 97H, HepG2 and Hep3B) were obtained from American Type Culture Collection (Manassas, VA, USA).

    Techniques: Transfection, Expressing, Northern Blot, Luciferase, Activity Assay, Reporter Assay

    miR-217 was involved in the regulation of HOTAIR on cell proliferation and cycle arrest in HepG2 cells. HepG2 cells were transfected with HOTAIR siRNA lentiviral vectors or miR-217 inhibitors, or the combination. (A) The proliferation rate was measured by CCK-8 assay. (B) The cell number was assessed by optical microscope. (C) The protein expression of Ki67, PCNA, p27 and cyclin D1 was evaluated by western blotting. (D) The cell cycle arrest was evaluated by flow cytometry (**P<0.01). HOTAIR, HOX transcript antisense RNA. miR-217, microRNA-217.

    Journal: Oncology Letters

    Article Title: HOTAIR contributes to the growth of liver cancer via targeting miR-217

    doi: 10.3892/ol.2018.8341

    Figure Lengend Snippet: miR-217 was involved in the regulation of HOTAIR on cell proliferation and cycle arrest in HepG2 cells. HepG2 cells were transfected with HOTAIR siRNA lentiviral vectors or miR-217 inhibitors, or the combination. (A) The proliferation rate was measured by CCK-8 assay. (B) The cell number was assessed by optical microscope. (C) The protein expression of Ki67, PCNA, p27 and cyclin D1 was evaluated by western blotting. (D) The cell cycle arrest was evaluated by flow cytometry (**P<0.01). HOTAIR, HOX transcript antisense RNA. miR-217, microRNA-217.

    Article Snippet: The normal human hepatic cell line HL-7702 and liver cancer cell lines (MHCC 97H, HepG2 and Hep3B) were obtained from American Type Culture Collection (Manassas, VA, USA).

    Techniques: Transfection, CCK-8 Assay, Microscopy, Expressing, Western Blot, Flow Cytometry

    HOTAIR inhibition suppresses tumor growth in xenograft models. Xenograft mouse model was created by subcutaneous injection of HepG2 cells pretreated with or without HOTAIR siRNA lentiviral vectors to nude mouse. (A) Five primary tumors from each group were photographed after sacrifice at 30th day. (B) Tumor growth curves in two groups were shown every 6 days until the 30th day following cells injection. (C and D) The expression of HPTAIR and miR-217 in primary tumor tissues was measured by qRT-PCR. (E and F) The expression of HPTAIR and miR-217 in primary tumor tissues was measured by northern blotting. (G and H) The expression of Ki67 and PCNA in primary tumor tissues was visualized by immunohistochemistry (*P<0.05, **P<0.01). HOTAIR, HOX transcript antisense RNA. miR-217, microRNA-217.

    Journal: Oncology Letters

    Article Title: HOTAIR contributes to the growth of liver cancer via targeting miR-217

    doi: 10.3892/ol.2018.8341

    Figure Lengend Snippet: HOTAIR inhibition suppresses tumor growth in xenograft models. Xenograft mouse model was created by subcutaneous injection of HepG2 cells pretreated with or without HOTAIR siRNA lentiviral vectors to nude mouse. (A) Five primary tumors from each group were photographed after sacrifice at 30th day. (B) Tumor growth curves in two groups were shown every 6 days until the 30th day following cells injection. (C and D) The expression of HPTAIR and miR-217 in primary tumor tissues was measured by qRT-PCR. (E and F) The expression of HPTAIR and miR-217 in primary tumor tissues was measured by northern blotting. (G and H) The expression of Ki67 and PCNA in primary tumor tissues was visualized by immunohistochemistry (*P<0.05, **P<0.01). HOTAIR, HOX transcript antisense RNA. miR-217, microRNA-217.

    Article Snippet: The normal human hepatic cell line HL-7702 and liver cancer cell lines (MHCC 97H, HepG2 and Hep3B) were obtained from American Type Culture Collection (Manassas, VA, USA).

    Techniques: Inhibition, Injection, Expressing, Quantitative RT-PCR, Northern Blot, Immunohistochemistry

    KRT19 binds a lincRNA Linc-KILH in HCC cells. (A) The expression level of KRT19 in HCC cell lines was detected by immunoblotting. (B) Huh7 cells were subjected to RIP assays with a KRT19 antibody or isotype-matched control IgG, RIP-Seq analysis showing average-normalized, log2 transformed FPKM value of KRT19-RIP and input. (C) The amount of Linc-KILH in the precipitates was analyzed by quantitative real-time PCR analysis. RNA enrichment indicates the RNA levels of Linc-KILH or GAPDH in the anti-KRT19 precipitates relative to those in the IgG precipitates. D, Biotin-labeled Linc-KILH and Linc-KILH-AS were incubated with Huh7 cell lysate, and KRT19 interaction was confirmed by Western blotting. * P < 0.05.

    Journal: International Journal of Biological Sciences

    Article Title: Linc-KILH potentiates Notch1 signaling through inhibiting KRT19 phosphorylation and promotes the malignancy of hepatocellular carcinoma

    doi: 10.7150/ijbs.52279

    Figure Lengend Snippet: KRT19 binds a lincRNA Linc-KILH in HCC cells. (A) The expression level of KRT19 in HCC cell lines was detected by immunoblotting. (B) Huh7 cells were subjected to RIP assays with a KRT19 antibody or isotype-matched control IgG, RIP-Seq analysis showing average-normalized, log2 transformed FPKM value of KRT19-RIP and input. (C) The amount of Linc-KILH in the precipitates was analyzed by quantitative real-time PCR analysis. RNA enrichment indicates the RNA levels of Linc-KILH or GAPDH in the anti-KRT19 precipitates relative to those in the IgG precipitates. D, Biotin-labeled Linc-KILH and Linc-KILH-AS were incubated with Huh7 cell lysate, and KRT19 interaction was confirmed by Western blotting. * P < 0.05.

    Article Snippet: Human HCC cell lines (SMMC-7721, Huh7, HepG2, MHCC-97H, MHCC-97L, Hep3B) and the human normal liver L02 cell line were obtained from KeyGen (Nanjing KeyGen Biotech Co., Ltd., Jiangsu, China).

    Techniques: Expressing, Western Blot, Transformation Assay, Real-time Polymerase Chain Reaction, Labeling, Incubation

    Linc-KILH is up-regulated in HCC tissues and correlated with the prognosis of patients with HCC. ( A) The expression level of Linc-KILH was detected by RT-qPCR in HCC tumor tissues and adjacent non-tumor liver tissues. (B) Relative expression of Linc-KILH in human L02 hepatocytes and HCC cell lines was detected by RT-qPCR. (C) The subcellular location of Linc-KILH was analyzed through fluorescence in situ hybridization (FISH) (original magnification ×400). (D) The overall survival and recurrence-free survival rates of 116 HCC patients were compared between higher Linc-KILH and lower Linc-KILH groups. *** P < 0.001.

    Journal: International Journal of Biological Sciences

    Article Title: Linc-KILH potentiates Notch1 signaling through inhibiting KRT19 phosphorylation and promotes the malignancy of hepatocellular carcinoma

    doi: 10.7150/ijbs.52279

    Figure Lengend Snippet: Linc-KILH is up-regulated in HCC tissues and correlated with the prognosis of patients with HCC. ( A) The expression level of Linc-KILH was detected by RT-qPCR in HCC tumor tissues and adjacent non-tumor liver tissues. (B) Relative expression of Linc-KILH in human L02 hepatocytes and HCC cell lines was detected by RT-qPCR. (C) The subcellular location of Linc-KILH was analyzed through fluorescence in situ hybridization (FISH) (original magnification ×400). (D) The overall survival and recurrence-free survival rates of 116 HCC patients were compared between higher Linc-KILH and lower Linc-KILH groups. *** P < 0.001.

    Article Snippet: Human HCC cell lines (SMMC-7721, Huh7, HepG2, MHCC-97H, MHCC-97L, Hep3B) and the human normal liver L02 cell line were obtained from KeyGen (Nanjing KeyGen Biotech Co., Ltd., Jiangsu, China).

    Techniques: Expressing, Quantitative RT-PCR, Fluorescence, In Situ Hybridization

    Linc-KILH promotes HCC cell proliferation in vitro . (A) Gene silence of Linc-KILH using Linc-KILH shRNAs in Huh7, MHCC-97H and Hep3B cells was conducted and the transfection efficiency was validated by RT-qPCR. (B) Cell proliferation assays for Huh7, MHCC-97H and Hep3B cells infected with the lentivirus silencing Linc-KILH or the control using Cell Counting Kit-8 assay. (C) EdU staining was used to detected the proliferation abilities of HCC cells knockdown of Linc-KILH (original magnification ×100). Each experiment was performed in triplicate and the results are shown as the means ± SD. * P < 0.05; ** P < 0.01.

    Journal: International Journal of Biological Sciences

    Article Title: Linc-KILH potentiates Notch1 signaling through inhibiting KRT19 phosphorylation and promotes the malignancy of hepatocellular carcinoma

    doi: 10.7150/ijbs.52279

    Figure Lengend Snippet: Linc-KILH promotes HCC cell proliferation in vitro . (A) Gene silence of Linc-KILH using Linc-KILH shRNAs in Huh7, MHCC-97H and Hep3B cells was conducted and the transfection efficiency was validated by RT-qPCR. (B) Cell proliferation assays for Huh7, MHCC-97H and Hep3B cells infected with the lentivirus silencing Linc-KILH or the control using Cell Counting Kit-8 assay. (C) EdU staining was used to detected the proliferation abilities of HCC cells knockdown of Linc-KILH (original magnification ×100). Each experiment was performed in triplicate and the results are shown as the means ± SD. * P < 0.05; ** P < 0.01.

    Article Snippet: Human HCC cell lines (SMMC-7721, Huh7, HepG2, MHCC-97H, MHCC-97L, Hep3B) and the human normal liver L02 cell line were obtained from KeyGen (Nanjing KeyGen Biotech Co., Ltd., Jiangsu, China).

    Techniques: In Vitro, Transfection, Quantitative RT-PCR, Infection, Cell Counting, Staining

    Linc-KILH enhances the migration and invasion abilities of HCC cells in vitro. (A and B) Transwell assays were conducted to examined the migration and invasion abilities of Huh7, MHCC-97H and Hep3B cells transfected with Linc-KILH shRNA (original magnification ×100). Each experiment was performed in triplicate and the results are shown as the means ± SD. * P < 0.05.

    Journal: International Journal of Biological Sciences

    Article Title: Linc-KILH potentiates Notch1 signaling through inhibiting KRT19 phosphorylation and promotes the malignancy of hepatocellular carcinoma

    doi: 10.7150/ijbs.52279

    Figure Lengend Snippet: Linc-KILH enhances the migration and invasion abilities of HCC cells in vitro. (A and B) Transwell assays were conducted to examined the migration and invasion abilities of Huh7, MHCC-97H and Hep3B cells transfected with Linc-KILH shRNA (original magnification ×100). Each experiment was performed in triplicate and the results are shown as the means ± SD. * P < 0.05.

    Article Snippet: Human HCC cell lines (SMMC-7721, Huh7, HepG2, MHCC-97H, MHCC-97L, Hep3B) and the human normal liver L02 cell line were obtained from KeyGen (Nanjing KeyGen Biotech Co., Ltd., Jiangsu, China).

    Techniques: Migration, In Vitro, Transfection, shRNA

    Linc-KILH facilitates HCC growth and metastasis in vivo . (A) Huh7 and Hep3B cells knockdown of Linc-KILH and the control cells were subcutaneously injected into 6-week-old BALB/c nude mice, 5 weeks later, the mice were sacrificed and the tumor size was measured. (B) The percentage of Ki-67 and PCNA positive staining cells was detected by immunohistochemistry in the tumor tissues from the subcutaneous xenograft model (original magnification ×100). (C) A lung metastasis model was established in which mice were injected with HCC cells (5 × 10 6 cells suspended in 200 µL PBS) through the tail vein and the lung metastasis was investigated respectively using the IVIS Lumina II system. Representative images of a mouse in each group were presented. (D) All the results of lung colonization were validated by the histological examination (H&E) (original magnification ×100). Metastatic tumors with volumes >2mm 3 were identified and compared in each group. Experiments were performed in triplicate independently and the results are shown as the means ± SD. * P < 0.05.

    Journal: International Journal of Biological Sciences

    Article Title: Linc-KILH potentiates Notch1 signaling through inhibiting KRT19 phosphorylation and promotes the malignancy of hepatocellular carcinoma

    doi: 10.7150/ijbs.52279

    Figure Lengend Snippet: Linc-KILH facilitates HCC growth and metastasis in vivo . (A) Huh7 and Hep3B cells knockdown of Linc-KILH and the control cells were subcutaneously injected into 6-week-old BALB/c nude mice, 5 weeks later, the mice were sacrificed and the tumor size was measured. (B) The percentage of Ki-67 and PCNA positive staining cells was detected by immunohistochemistry in the tumor tissues from the subcutaneous xenograft model (original magnification ×100). (C) A lung metastasis model was established in which mice were injected with HCC cells (5 × 10 6 cells suspended in 200 µL PBS) through the tail vein and the lung metastasis was investigated respectively using the IVIS Lumina II system. Representative images of a mouse in each group were presented. (D) All the results of lung colonization were validated by the histological examination (H&E) (original magnification ×100). Metastatic tumors with volumes >2mm 3 were identified and compared in each group. Experiments were performed in triplicate independently and the results are shown as the means ± SD. * P < 0.05.

    Article Snippet: Human HCC cell lines (SMMC-7721, Huh7, HepG2, MHCC-97H, MHCC-97L, Hep3B) and the human normal liver L02 cell line were obtained from KeyGen (Nanjing KeyGen Biotech Co., Ltd., Jiangsu, China).

    Techniques: In Vivo, Injection, Staining, Immunohistochemistry

    Linc-KILH inhibits the phosphorylation of KRT19 to potentiate Notch1 signaling in HCC. (A) The expression levels of total and phosphorylated KRT19 on Ser35 site in Huh7, MHCC-97H and Hep3B cells upon Linc-KILH alteration were examined by western blotting. (B) The subcellular location and the content of the phosphorylated and total KRT19 were detected by western blotting in KRT19 positive Huh7 and MHCC-97H cells. (C) Co-immunoprecipitation (Co-IP) was performed using Protein A/G Sepharose and antibodies specific for KRT19, β-catenin, and RAC1, or normal IgG in KRT19 positive Huh7 and MHCC-97H cells. Cell lysates were analyzed by Western blotting. (D) Cell fractionation assay for β-catenin and RAC1 analyzed by Western blotting; actin and c-Jun were used as the cytoplasmic and nuclear markers, respectively, in KRT19 positive Huh7 and MHCC-97H cells. (E) The variation of the expression of the members of Nothc1 signaling pathway in Linc-KILH-silenced cells was determined by western blotting. (F) The expression levels of cell proliferation and EMT transformation related genes were examined by western blotting in HCC cells upon Linc-KILH silence.

    Journal: International Journal of Biological Sciences

    Article Title: Linc-KILH potentiates Notch1 signaling through inhibiting KRT19 phosphorylation and promotes the malignancy of hepatocellular carcinoma

    doi: 10.7150/ijbs.52279

    Figure Lengend Snippet: Linc-KILH inhibits the phosphorylation of KRT19 to potentiate Notch1 signaling in HCC. (A) The expression levels of total and phosphorylated KRT19 on Ser35 site in Huh7, MHCC-97H and Hep3B cells upon Linc-KILH alteration were examined by western blotting. (B) The subcellular location and the content of the phosphorylated and total KRT19 were detected by western blotting in KRT19 positive Huh7 and MHCC-97H cells. (C) Co-immunoprecipitation (Co-IP) was performed using Protein A/G Sepharose and antibodies specific for KRT19, β-catenin, and RAC1, or normal IgG in KRT19 positive Huh7 and MHCC-97H cells. Cell lysates were analyzed by Western blotting. (D) Cell fractionation assay for β-catenin and RAC1 analyzed by Western blotting; actin and c-Jun were used as the cytoplasmic and nuclear markers, respectively, in KRT19 positive Huh7 and MHCC-97H cells. (E) The variation of the expression of the members of Nothc1 signaling pathway in Linc-KILH-silenced cells was determined by western blotting. (F) The expression levels of cell proliferation and EMT transformation related genes were examined by western blotting in HCC cells upon Linc-KILH silence.

    Article Snippet: Human HCC cell lines (SMMC-7721, Huh7, HepG2, MHCC-97H, MHCC-97L, Hep3B) and the human normal liver L02 cell line were obtained from KeyGen (Nanjing KeyGen Biotech Co., Ltd., Jiangsu, China).

    Techniques: Expressing, Western Blot, Immunoprecipitation, Co-Immunoprecipitation Assay, Cell Fractionation, Transformation Assay

    KRT19 is essential for the tumor promoting function of Linc-KILH in HCC. (A) EdU staining was used to detected the proliferation abilities of HCC cells when Linc-KILH was overexpressed with and without KRT19 silence in Huh7 cells (original magnification ×100). (B) Transwell assays were conducted to examined the migration and invasion abilities of Linc-KILH overexpressed Huh7 cells upon KRT19 silence (original magnification ×100). (C) Images and volume of xenografts established by subcutaneous transplantation with Linc-KILH overexpression and KRT19 knockdown were exhibited and calculated. (D) Representative images of the lung metastasis model and the luciferase activities were measured by IVIS imaging system. Each experiment was performed in triplicate and the results are shown as the means ± SD. * P < 0.05.

    Journal: International Journal of Biological Sciences

    Article Title: Linc-KILH potentiates Notch1 signaling through inhibiting KRT19 phosphorylation and promotes the malignancy of hepatocellular carcinoma

    doi: 10.7150/ijbs.52279

    Figure Lengend Snippet: KRT19 is essential for the tumor promoting function of Linc-KILH in HCC. (A) EdU staining was used to detected the proliferation abilities of HCC cells when Linc-KILH was overexpressed with and without KRT19 silence in Huh7 cells (original magnification ×100). (B) Transwell assays were conducted to examined the migration and invasion abilities of Linc-KILH overexpressed Huh7 cells upon KRT19 silence (original magnification ×100). (C) Images and volume of xenografts established by subcutaneous transplantation with Linc-KILH overexpression and KRT19 knockdown were exhibited and calculated. (D) Representative images of the lung metastasis model and the luciferase activities were measured by IVIS imaging system. Each experiment was performed in triplicate and the results are shown as the means ± SD. * P < 0.05.

    Article Snippet: Human HCC cell lines (SMMC-7721, Huh7, HepG2, MHCC-97H, MHCC-97L, Hep3B) and the human normal liver L02 cell line were obtained from KeyGen (Nanjing KeyGen Biotech Co., Ltd., Jiangsu, China).

    Techniques: Staining, Migration, Transplantation Assay, Over Expression, Luciferase, Imaging