Clinicopathological features, prognostic significance, and associated tumor cell functions of family with sequence similarity 111 member B in pancreatic adenocarcinoma

Abstract

Backgroud Among digestive tract tumors, pancreatic adenocarcinoma (PAAD) has a high degree of malignancy. Therefore, it is important to search for pancreatic adenocarcinoma‐related differential genes and new oncogene therapeutic targets for early diagnosis, treatment, and prognosis of pancreatic adenocarcinoma. Aims This study aims to investigate the expression and clinical significance of Family with sequence similarity 111 member B (FAM111B) in PAAD. Materials & Methods Bioinformatics was used to analyze the relationship between FAM111B expression and pancreatic adenocarcinoma and to predict its role in related pathways. Tissue microarrays were used to assess the levels of FAM111B in pancreatic cancer tissues by immunohistochemical staining, and the effects of FAM111B expression levels on apoptosis, proliferation, invasion and migration of tumor cells were observed and verified by in vitro cellular assays. Results FAM111B expression was higher in PAAD tissue than in matched normal tissues (p < 0.05). The expression level of FAM111B, the metastatic status of lymph nodes was an independent prognostic factor for PAAD survival (p < 0.05). Meanwhile, overexpression of FAM111B promoted PAAD cell proliferation, migration, invasion and inhibited PAAD cell apoptosis (p < 0.05). In contrast, knockdown of FAM111B triggered the opposite result (p < 0.05). In the results of GSEA, it was shown that FAM111B may be involved in PAAD progression through p53 signaling pathway, cell cycle, and other signaling pathways (p < 0.05 and FDR q‐val <0.25). FAM111B is highly expressed in PAAD tissues and is closely associated with poor prognosis of PAAD. Conclusion FAM111B significantly promotes the proliferation, invasion, and migration of pancreatic adenocarcinoma cells while it inhibits their apoptosis. FAM111B may be a new biomarker for PAAD. It may provide a new direction for the treatment and diagnosis of PAAD.

CENPN contributes to pancreatic carcinoma progression through the MDM2-mediated p53 signaling pathway

“…Knockdown of CENPN resulted in suppressed cell growth, migration, and invasion of PAAD cells, whereas upregulation of CENPN significantly promoted cell proliferation, invasion, and migration. As the p53 signaling pathway is known to be related to the pathogenesis of PAAD [12,41], we analyzed the possible effects of CENPN in combination with this pathway. Western blot analysis showed that downregulation of CENPN in PAAD cells upregulated the expression of MDM2 and downregulated the expression of p53 and its downstream target p21, indicating that CENPN may play a role in regulating the P53 pathway in PAAD.…”

Family with sequence similarity 111 member B contributes to tumor growth and metastasis by mediating cell proliferation, invasion, and EMT via transforming acidic coiled‐coil protein 3/PI3K/AKT signaling pathway in hepatocellular carcinoma

“…For example, Xiang and colleagues found that FAM111B was lowly expressed in papillary thyroid cancer (PTC) tissues, leading to poor prognosis in PTC patients 4 . In addition, the over‐activation of FAM111B in pancreas, lung, cervix and breast increased the risk of related‐cancer 5–9 . Boldanova et al revealed that FAM111B was highly expressed in the tumor region of HCC patients and could be used as a biomarker for HCC patients treated with transarterial chemoembolization 10 .…”

“…4 In addition, the over-activation of FAM111B in pancreas, lung, cervix and breast increased the risk of related-cancer. [5][6][7][8][9] Boldanova et al revealed that FAM111B was highly expressed in the tumor region of HCC patients and could be used as a biomarker for HCC patients treated with transarterial chemoembolization. 10 Therefore, the course of HCC may have an inseparable relationship with FAM111B.…”