Association of miR-9-5p and NFIC in the progression of gastric cancer

Abstract

Background Gastric cancer is the most common malignant neoplasm of digestive system. Herein, we aim to detect the expression of nuclear factor I C (NFIC) in gastric cancer cells, and to explore the effect and mechanism of its expression on the development of gastric cancer. Methods qPCR and Western blot assays were carried out to detect NFIC expression. Then, BGC-823 and SGC-7901 cell lines were selected to perform the following functional experiments. The function of NFIC on gastric cancer cells was analyzed by biological experiments. The associations between miR-9-5p and NFIC were searched on the bioinformatics website and identified by dual luciferase assay. The effects of miR-9-5p and NFIC on cells were verified by co-transfection experiments. The related genes expression was examined by Western blot. Results A marked augmentation of NFIC was observed in gastric cancer cells. Knockdown of NFIC significantly inhibited the viability, colony formation, invasion, and migration of gastric cancer cells. Overexpression of miR-9-5p obviously suppressed the viability, colony formation, invasion, and migration of gastric cancer cells, and this phenomenon was aggravated by si-NFIC. Additionally, the expression levels of PCNA, vimentin, and Snail were obviously decreased after miR-9-5p mimic or/and si-NFIC treatment. Conclusions These results suggested that NFIC was highly expressed in gastric cancer cells, and knockdown of NFIC suppressed the growth and mobility of gastric cancer cells; miR-9-5p was identified as an upstream regulator of NFIC and suppressed the malignant behaviors of gastric cancer cells by targeting NFIC through affecting PCNA, vimentin, and Snail expression.

Pan‐cancer analyses reveal molecular and clinical characteristics of cuproptosis regulators

“…It is important to mention that the TF NFIC targets nine cuproptosis regulators in the regulatory network, implying that NFIC may be a key upstream TF of cuproptosis. The role of NFIC in the regulation of growth and metastasis of a variety of tumors has been confirmed, and its mechanism involves the EMT process and nuclear factor kappa B pathway [ 62 , 63 , 64 , 65 , 66 , 67 ]. However, the association of NFIC with cuproptosis activity has never been characterized; therefore, we hypothesized that NFIC could also affect tumor development by regulating cuproptosis activity, which deserves further exploration.…”

MiR‐9 promotes G‐MDSC recruitment and tumor proliferation by targeting SOCS3 in breast cancer

“…15,16 Our recent research demonstrated that miR-9 can augment the tumor-initiating potential of breast cancer cells through a transgenic mouse model. 17 Nevertheless, in the context of lung, 18 gastric, 19 and pancreatic 20 cancers, miR-9 might function as a tumor suppressor. Nonetheless, the intricate mechanisms through which miR-9 modulates the immune microenvironment in breast cancer remain incompletely elucidated.…”