Fig. 5: MTCH2 silencing inhibits the proliferative and migratory capacities of primary human CRPC cells. | Cell Death & Disease

Fig. 5: MTCH2 silencing inhibits the proliferative and migratory capacities of primary human CRPC cells.

From: Identification of mitochondrial carrier homolog 2 as an important therapeutic target of castration-resistant prostate cancer

Fig. 5

The primary pPC-1 cells were subjected to individual treatments with specific MTCH2 shRNAs (shMTCH2-S1, shMTCH2-S2, or shMTCH2-S3, each representing a unique sequence) or a control scramble non-sense shRNA (c-sh), the stable cells were formed after puromycin selection. The equal number of cells were cultured for designated time periods, and various cellular functions, including colony formation (A), cell proliferation (measured by the percentage of EdU-incorporated nuclei, B), cell viability (assessed by CCK-8 optical density, C), in vitro cell migration (analyzed using “Transwell” assays, D), and cell invasion (examined via “Matrigel Transwell” assays, E) were measured. Additionally, stable cells derived from other primary CRPC cells (pPC-2, pPC-3, and pPC-4) as well as the primary human prostate epithelial cells (pEpi1 and pEpi2) expressing either c-sh or shMTCH2-S1 were established and MTCH2/MTCH1 mRNA expression was examined (I, J); Equal cell numbers were cultured for designated time periods, cell viability (F, K), proliferation (G, L) and migration (H) were measured similarly. The data are expressed as mean ± standard deviation (SD, n = 5). “Ctrl” denotes the parental control cells. Statistical significance is marked by *P < 0.05 when compared to “c-sh” cells. “n.s.” denotes non-statistically significant differences (P > 0.05). The experiments depicted in this figure were conducted five times (biological replicates), consistently producing similar results. The scale bar represents 100 μm.

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