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MIR4435-2HG is upregulated in HCC, predicts poor prognosis, and promotes malignant phenotypes ( A ) Analysis of the TCGA-LIHC dataset shows significant upregulation of MIR4435-2HG in HCC tissues compared to adjacent non-tumor tissues. ( B ) Kaplan-Meier analysis of overall survival in HCC patients stratified by MIR4435-2HG expression using the median cutoff (50th percentile, n = 182 per group). ( C <t>)</t> <t>qRT-PCR</t> analysis confirms high expression of MIR4435-2HG in a panel of HCC cell lines. ( D ) CCK-8 assays in PLC/PRF5 and Huh7 cells demonstrate that knockdown of MIR4435-2HG suppresses proliferation, while its overexpression enhances proliferation. ( E ) The half-maximal inhibitory concentration (IC₅₀) of lenvatinib in parental and resistant PLC/PRF5 and Huh7 cells. ( F ) MIR4435-2HG expression is further elevated in acquired lenvatinib-resistant HCC cells (Huh7-L-R, PLC/PRF5-L-R) compared to their parental counterparts. ( G ) Transwell migration and invasion assays show that knockdown of MIR4435-2HG reduces, while its overexpression enhances, migratory and invasive capabilities in lenvatinib-resistant PLC/PRF5 and Huh7 cells. Data are presented as mean ± SD; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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MIR4435-2HG is upregulated in HCC, predicts poor prognosis, and promotes malignant phenotypes ( A ) Analysis of the TCGA-LIHC dataset shows significant upregulation of MIR4435-2HG in HCC tissues compared to adjacent non-tumor tissues. ( B ) Kaplan-Meier analysis of overall survival in HCC patients stratified by MIR4435-2HG expression using the median cutoff (50th percentile, n = 182 per group). ( C ) qRT-PCR analysis confirms high expression of MIR4435-2HG in a panel of HCC cell lines. ( D ) CCK-8 assays in PLC/PRF5 and Huh7 cells demonstrate that knockdown of MIR4435-2HG suppresses proliferation, while its overexpression enhances proliferation. ( E ) The half-maximal inhibitory concentration (IC₅₀) of lenvatinib in parental and resistant PLC/PRF5 and Huh7 cells. ( F ) MIR4435-2HG expression is further elevated in acquired lenvatinib-resistant HCC cells (Huh7-L-R, PLC/PRF5-L-R) compared to their parental counterparts. ( G ) Transwell migration and invasion assays show that knockdown of MIR4435-2HG reduces, while its overexpression enhances, migratory and invasive capabilities in lenvatinib-resistant PLC/PRF5 and Huh7 cells. Data are presented as mean ± SD; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Journal: Cancer Cell International

Article Title: Targeting the MIR4435-2HG/miR-29c-3p/FSP1 axis overcomes lenvatinib resistance by inducing ferroptosis in hepatocellular carcinoma

doi: 10.1186/s12935-025-04147-5

Figure Lengend Snippet: MIR4435-2HG is upregulated in HCC, predicts poor prognosis, and promotes malignant phenotypes ( A ) Analysis of the TCGA-LIHC dataset shows significant upregulation of MIR4435-2HG in HCC tissues compared to adjacent non-tumor tissues. ( B ) Kaplan-Meier analysis of overall survival in HCC patients stratified by MIR4435-2HG expression using the median cutoff (50th percentile, n = 182 per group). ( C ) qRT-PCR analysis confirms high expression of MIR4435-2HG in a panel of HCC cell lines. ( D ) CCK-8 assays in PLC/PRF5 and Huh7 cells demonstrate that knockdown of MIR4435-2HG suppresses proliferation, while its overexpression enhances proliferation. ( E ) The half-maximal inhibitory concentration (IC₅₀) of lenvatinib in parental and resistant PLC/PRF5 and Huh7 cells. ( F ) MIR4435-2HG expression is further elevated in acquired lenvatinib-resistant HCC cells (Huh7-L-R, PLC/PRF5-L-R) compared to their parental counterparts. ( G ) Transwell migration and invasion assays show that knockdown of MIR4435-2HG reduces, while its overexpression enhances, migratory and invasive capabilities in lenvatinib-resistant PLC/PRF5 and Huh7 cells. Data are presented as mean ± SD; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Article Snippet: Kaplan-Meier survival analysis indicates that high FSP1 expression is strongly associated with poorer overall survival in HCC patients. ( D ) Immunohistochemistry data from The Human Protein Atlas demonstrates elevated FSP1 protein expression in HCC specimens. ( E, F ) Experimental validation of FSP1 upregulation in HCC cell lines at the mRNA ( E ) and protein ( F ) levels. ( G ) qRT-PCR analysis revealed the regulatory role of MIR4435-2HG on FSP1 mRNA expression.

Techniques: Expressing, Quantitative RT-PCR, CCK-8 Assay, Knockdown, Over Expression, Concentration Assay, Migration