Downregulation of CDCA3 expression inhibits tumor formation in pancreatic cancer.

Downregulation of cell division cycle-associated 3 (CDCA3) markedly inhibited cell growth and induced apoptosis in tumors. However, the effect of CDCA3 in pancreatic cancer (PAC) was rarely investigated. Therefore, this study attempted to clarify the role of CDCA3 in PAC. The mRNA and protein expression of CDCA3 were examined in PAC cell lines and tumor tissues by using real-time quantitative PCR (RT-qPCR), western blotting (WB), and immunohistochemistry (IHC). The effects of CDCA3 downregulation on cell proliferation, apoptosis, and colony information were investigated through MTT assay, Annexin V-APC single staining cell apoptosis detection, and colony formation test. The microarray and ingenuity pathway analysis were employed to explore the potential regulatory relation. The tumor xenograft model was established for determining the effect of CDCA3 downregulation on the growth of PAC in vivo. The results showed that the expression of CDCA3 in tumor tissues was higher than that of normal tissues (p<0.05). In addition, the mRNA expression of CDCA3 was markedly increased in PANC-1 cells and SW 1990 cells when compared with human pancreatic duct epithelial (HPDE) cells (p<0.05). MTT assay showed that the cell proliferation of PANC-1 cells and SW 1990 cells was significantly inhibited after the lentivirus transfection of CDCA3 knockdown (p<0.05). Annexin V-APC apoptosis assays suggested that the apoptotic cell number was markedly increased in the shCDCA3 group compared to that in the shCtrl group in SW 1990 cells and PANC-1 cells (p<0.05). Meanwhile, the activity of caspase-3/7 was obviously elevated in the shCDCA3 group compared to the shCtrl group (p<0.05). The colony formation was notably inhibited in the shCDCA3 group relative to the shCtrl group in SW 1990 cells (p<0.05). Moreover, the tumor growth was evidently suppressed in the shCDCA3 group compared with the shCtrl group in vivo (p<0.05). These findings revealed that CDCA3 plays a crucial role in the progress of PCA by regulating cell apoptosis and proliferation, which may serve as a potential target for PAC treatment.

Upregulation of miR-3658 in bladder cancer and tumor progression.

Despite increasing advances in surgical techniques and adjuvant chemotherapies, bladder cancer remains the ninth leading cause of male malignancy-associated deaths worldwide. Several microRNAs (miRNAs) have been identified to be closely associated with the progression and prognosis of, and response to treatments in various human cancers. However, few studies have investigated the role of miR-3658 in bladder cancer. In this study, we examined the expression of miR-3658 in 96 pairs of bladder cancer tissues and adjacent non-tumor tissues via quantitative reverse-transcription polymerase chain reaction. Results showed that expression of miR-3658 was up-regulated in the bladder cancer tissues as compared with that in the corresponding control tissues (4.15 ± 2.78 vs 2.17 ± 1.14; P < 0.0001). Furthermore, higher miR-3658 expression was significantly associated with lymph node invasion, distant metastasis, histological grade, TNM stage, and tumor recurrence in bladder cancer (all P < 0.0001). miR-3658 expression was not associated with other clinicopathological variables such as age, gender, tumor size, and number (all P > 0.05). Our study revealed that miR-3658 overexpression is involved in tumor progression of bladder cancer, indicating that the miRNA possesses prognostic values.