CCNI2 knockdown inhibits the proliferation, apoptosis and migration of pancreatic cancer cells

作者：Bingyang Hu, Wenzhi Zhang, Changsheng Zhang, Chonghui Li, Ning Zhang, Ke Pan, Xinlan Ge, Tao Wan · 发表于：Research Square (Research Square) · 年份：2020 · DOI：10.21203/rs.3.rs-24690/v1 · 研究领域：Liver physiology and pathology、Cancer Mechanisms and Therapy、Wnt/β-catenin signaling in development and cancer

Abstract Background: Pancreatic cancer has been recognized as one of the most serious malignant tumors in the world, and its molecular mechanism is still not fully understood. Cyclin I-like (CCNI2) is a homolog of Cyclin I (CCNI), and at present its function is largely unknown.Methods: In this study, we aimed to explore the role of CCNI2 in the development of pancreatic cancer. The expression levels of CCNI2 in pancreatic cancer tissues and cells were detected by immunohistochemical analysis and qPCR, respectively. Lentivirus was used to deliver shRNA to pancreatic cancer cells to construct CCNI2 knockdown cell models. MTT and colony formation assays were used to assess cell proliferation capacity, flow cytometry was used to detect apoptosis, wound-healing and Transwell assays were used to determine cell migration.Results: Our results revealed that CCNI2 is not only highly expressed in pancreatic cancer, but also significantly correlated with pathological grade, pathological stage, and survival rate. It was confirmed that knockdown of CCNI2 inhibited the proliferation and cell migration of pancreatic cancer cells while promoting apoptosis. Furthermore, human apoptotic antibody arrays showed that CCNI2 is involved in apoptosis process by up-regulating the pro-apoptotic proteins.Conclusions: In conclusion, CCNI2 may be a prognostic marker for pancreatic cancer and is associated with its development. Thus, CCNI2 possesses potential to act as a therapeutic target for pancreatic c...