Alterations of mitochondrial DNA (mtDNA) have been associated with the risk of a number of human cancers; however, the relationship between mtDNA copy number in peripheral blood leukocytes (PBLs) and the risk of prostate cancer (PCa) has not been investigated. In a case-control study of 196 PCa patients and 196 age-paired healthy controls in a Chinese Han population, the association between mtDNA copy number in PBLs and PCa risk was evaluated. The relative mtDNA copy number was measured using quantitative real-time PCR; samples from three cases and two controls could not be assayed, leaving 193 cases and 194 controls for analysis. PCa patients had significantly higher mtDNA copy numbers than controls (medians 0.91 and 0.82, respectively; P<0.001). Dichotomized at the median value of mtDNA copy number in the controls, high mtDNA copy number was significantly associated with an increased risk of PCa (adjusted odds ratio  = 1.85, 95% confidence interval: 1.21–2.83). A significant dose-response relationship was observed between mtDNA copy number and risk of PCa in quartile analysis (P trend = 0.011). Clinicopathological analysis showed that high mtDNA copy numbers in PCa patients were significantly associated with high Gleason score and advanced tumor stage, but not serum prostate-specific antigen level (P = 0.002, 0.012 and 0.544, respectively). These findings of the present study indicate that increased mtDNA copy number in PBLs is significantly associated with an increased risk of PCa and may be a reflection of tumor burden.

Kruppel-like factor 9 (KLF9), a transcription factor, is critical for the inhibition of growth and development of tumors, whereas its effects in pancreatic cancer remains unclear. The purpose of the present study was to investigate the expression and functional significance of KLF9 in vitro, by assessing the expression of KLF9 in pancreatic cancer tissue samples and its association with the total survival of patients and clinicopathological data. The levels of KLF9 expression in adjacent tissues and pancreatic cancer tissues were detected using immunohistochemistry. Using western blot analyses, we assessed KLF9 expression in human pancreatic cancer cell lines. Using flow cytometric analysis and CCK-8, we evaluated the effects of KLF9 expression on cell apoptosis, the cell cycle and proliferation of pancreatic cancer cells. Its effects on migration and cell invasion were detected by performing Transwell assay. By conducting western blot analyses, we evaluated the expression of relative target proteins (involved in invasion, migration, apoptosis, and cell cycle distribution. Our results revealed that in both tissue samples and cell lines (particularly in BxPC-3 and PANC-1 cells) of pancreatic cancer, KLF9 exhibited relatively lower expression. In addition, low KLF9 expression was related to the differentiation (P<0.001) and depth of vascular invasion (P=0.016) and was associated with a poor overall survival rate. In PANC-1 and BxPC-3 cells, KLF9 overexpression decreased the proliferation of pancreatic cancer cells, induced apoptosis, blocked the cell cycle at the S phase, and inhibited the migration and invasion of tumor cells. KLF9 overexpression downregulated MMP-9, MMP-2 Bcl-2, N-cadherin and cyclin B, and upregulated the levels of E-cadherin, Bax, p53, CDK4 and cyclin D1. On the whole, our findings indicated that KLF9 exhibited low expression in pancreatic cancer, and upregulation of KLF9 may inhibit the progression of pancreatic cancer. KLF9 may have potential diagnostic and therapeutic values in this type of cancer.

Prostate cancer (PC) is a prevalent male malignancy with high occurrence rate. Recent studies have showed that small nucleolar host genes (SNHGs) and their homolog small nucleolar RNAs (snoRNAs) elicit regulatory functions in carcinogenesis. Present study aimed to investigate the role of SNHG17 and its homolog SNORA71B in PC. Function of SNHG17 and SNORA71B in PC is detected by CCK-8, colony formation, flow cytometry analysis of apoptosis, and transwell migration assay. The mechanism whereby SNHG17 regulated SNORA71B was detected by RIP, pulldown, ChIP, and luciferase reporter assays. Results depicted that transcript 6 of SNHG17 and SNORA71B were upregulated in PC. Knockdown of SNHG17 or SNORA71B weakened proliferation, invasion, migration, and epithelial-to-mesenchymal transition (EMT) and strengthened apoptosis. Mechanistically, SNHG17 and SNORA71B were transcriptionally activated by signal transducer and activator of transcription 5A (STAT5A). SNHG17 positively regulated SNORA71B in PC cell lines and other cell lines. SNHG17 sponged miR-339-5p to upregulate STAT5A and therefore to cause transactivation of SNORA71B. Rescue experiments delineated that SNORA71B was required for the regulation of SNHG17 on PC. Moreover, SNHG17 silence hindered tumorigenesis of PC in vivo. In conclusion, current study first revealed that lncRNA SNHG17 aggravated prostate cancer progression through regulating its homolog SNORA71B via a positive feedback loop, which might do help to the pursuit of better PC treatment.