Fig 1: Downregulation of HM13 suppresses the proliferation of breast cancer in vitro and in vivo.A, B The transfection efficiencies of si-HM13-1 and si-HM13-2 were evaluated by qRT-PCR (A) and western blot (B) in SUM1315 and ZR-75-1 cell lines. C The CCK-8 assays were performed to measure the cell viability of SUM1315 (left) and ZR-75-1 (right) cell lines transfected with siRNAs. D Representative results of the colony formation showed the cell proliferation in SUM1315 and ZR-75-1 cell lines after downregulation of HM13. E, F EdU assays were conducted to compare the growth rates in SUM1315 (E) and ZR-75-1 (F) cell lines between experimental groups (si-HM13-1 and si-HM13-2) and control group (si-NC). DAPI was indicated by blue, EdU was indicated by red. Scale bars, 50 µm. G Images of xenograft tumors from nude mice classified into HM13 knockdown (sh-HM13) group and control (sh-NC) group (n = 6). H, I Average tumor volume (H) and tumor weight (I) of breast cancer in knockdown of HM13 (sh-HM13) and control (sh-NC) group were shown by tumor growth curves. J IHC staining of breast cancer tissues from tumor subcutaneous mice model was aimed to determine the positive rates of HM13 and Ki-67 in knockdown of HM13 (sh-HM13) and control (sh-NC) group. Scale bars, 100 µm. Data were shown as mean ± SD, (*p < 0.05, **p < 0.01, ***p < 0.001).
Fig 2: The expression level and clinical significance of HM13 in hepatocellular carcinoma (HCC). (A). The mRNA expression of HM13 in ICGC cohort. (B). Based on the ICGC cohort, Kaplan-Meier plot was used to evaluate the relationship between the expression of HM13 and overall survival. (C). Univariate and multivariate COX analyses were carried out to determine the effect of HM13 on overall survival. (D). The protein level of HM13 in CPTAC cohort. (E). Based on the CPTAC cohort, Kaplan-Meier plot was used to evaluate the relationship between the expression of HM13 and overall survival. (F). Univariate and multivariate COX analyses were carried out to determine the effect of HM13 on overall survival.
Fig 3: Downregulated HM13 inhibits PI3K-AKT-mTOR pathway in breast cancer.A Western blot assessment of PI3K, p-PI3K, AKT, p-AKT, mTOR, p-mTOR protein expression was performed in SUM1315 and ZR-75-1 cell lines with siRNAs (si-HM13-1 and si-HM13-2) or negative control (si-NC). B, D The effects of IGF-1 on cell proliferation were detected by CCK-8 (B) and EdU (C, D) assays. SUM1315 and ZR-75-1 cell lines were transfected with negative control (si-NC), siRNA (si-HM13) or siRNA and IGF-1 (si+IGF-1) before harvesting. Scale bars, 50 µm. E, F The wound healing assays were performed to determine the migration abilities of SUM1315 (E) and ZR-75-1 (F) transfected with negative control (si-NC), siRNA (si-HM13) or siRNA and IGF-1 (si+IGF-1). Scale bars, 100 µm. Data were shown as mean ± SD, *p < 0.05, **p < 0.01.
Fig 4: The effect of HM13 knockdown on Huh-7 cells functions. Huh-7 cell proliferation was measured by CCK8 assay (A) and colony formation (B). (C,D). Cell migration was determined by scratch wound assay. (E). Cell migration and invasion were determined by transwells assay. Experiments were repeated three times; *p < 0.05, **p < 0.01, ***p < 0.001.
Fig 5: Correlation analysis for HM13 expression with immune cell infiltration levels, immune checkpoints, and RNA modification-related molecules. (A). The correlation between HM13 expression and tumor infiltration levels was based on the TIMER database. (B). Pan-cancer co-expression analysis for HM13 and immune checkpoint genes. (C). Co-expression analysis for HM13 and RNA modification-related molecules. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
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