NFIB promotes the progression of gastric cancer by upregulating circMAP7D1 to stabilize HER2 mRNA

The present study evaluated the expression levels of nuclear factor I B (NFIB) in gastric cancer (GC) specimens and cells, and its regulatory roles were further elucidated. The expression levels of NFIB were examined in GC and paired normal specimens, and in human GC and normal gastric epithelial cells by reverse transcription‑quantitative PCR. A circular RNA (circRNA) microarray was performed to identify the novel downstream circRNA of NFIB. Cell proliferation was determined by Cell Counting Kit‑8 assay. Furthermore, cell cycle distribution and apoptosis were assessed using flow cytometry. Interactions between RNA were examined by RNA pulldown assay and the stability of target mRNA was evaluated using a mRNA stability assay. The results of the present study revealed that NFIB was upregulated in GC. Furthermore, silencing NFIB suppressed the proliferation of GC cells, whereas cell cycle arrest and apoptosis were enhanced. In addition, significant downregulation of circMAP7D1 (hsa_circ_0004093) was observed in GC cells infected with short hairpin RNA‑NFIB. These findings indicated that circMAP7D1 may be a promising downstream molecule of NFIB in GC, and further functional analyses indicated that circMAP7D1 was involved in NFIB‑modulated GC cell proliferation and apoptosis. Moreover, human epidermal growth factor receptor 2 (HER2) was identified as a novel target of circMAP7D1 in GC, and NFIB was able to increase the stability of HER2 mRNA through regulating circMAP7D1. In conclusion, the present findings indicated that NFIB expression was increased in GC. In addition, NFIB may promote the proliferation of GC cells and function through stabilizing HER2 mRNA by upregulating circMAP7D1. Notably, NFIB and its novel downstream signaling pathway may serve essential roles during the development of GC, and NFIB may be considered a promising candidate for the treatment of patients with GC.