fig2

LINC01607 promotes hepatocellular carcinoma progression and ferroptosis-associated therapy resistance with functional involvement of the p62–Keap1–Nrf2 pathway

Figure 2. LINC01607 promotes HCC cell proliferation and tumor growth. (A-C) Cell proliferation was evaluated by CCK-8 (A), colony formation (B), and EdU incorporation (C) assays. LINC01607 overexpression enhanced proliferative capacity, while two independent siRNAs targeting LINC01607 produced the opposite effect. Quantification of colony formation and EdU-positive cells is shown below the representative images; (D) Representative bioluminescence images and gross tumor images of the HCC orthotopic model at the experimental endpoint. The heatmap depicts the photon flux emitted from tumors. Tumors were excised, and tumor weights were statistically analyzed (n = 6); (E) Subcutaneous xenografts were established in BALB/c nude mice using Hep3B-WT cells with LINC01607 overexpression or vector control. Tumor size was tracked during the experiment, and final tumor weights were measured at the endpoint; (F) Representative histological images of HCC tumor xenografts stained with H&E and Ki-67 IHC. LINC01607 overexpression increased tumor cellularity and Ki-67 expression, indicating enhanced proliferation. Data are presented as mean ± SD. For cell-based assays, n = 3 independent biological replicates unless otherwise indicated. For animal experiments, n = 6 mice per group. Statistical significance was assessed using two-tailed Student’s t-test for two-group comparisons and one-way ANOVA for multiple-group comparisons. **P < 0.01, ***P < 0.001. HCC: Hepatocellular carcinoma; CCK-8: Cell Counting Kit-8; EdU: 5-ethynyl-2′-deoxyuridine; H&E: hematoxylin and eosin; IHC: immunohistochemistry; SD: standard deviation; ANOVA: analysis of variance.

Cancer Drug Resistance
ISSN 2578-532X (Online)

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