ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis

Zhang

et al. 2020

Preprint

Background: Oral cancer is a malignant disease threatening human’s life and greatly reduces human’s life quality. ANLN was reported to promote progression in cancer. This study aims at investigating the role of ANLN and the molecular mechanism in oral cancer. Methods: ANLN was down-regulated by RNAi technology. The effect of ANLN on cell behaviors including proliferation, cycle distribution, invasion, and apoptosis was detected. Western blotting analysis was used to explore the mechanism of ANLN in oral cancer. Results: Based on data from TCGA database, ANLN was shown to be expressed significantly higher in tumor tissues than the normal control. Patients with higher ANLN expression exhibited shorter survival time. ANLN was also expressed abundantly in cancer cell lines CAL27 and HN30. When ANLN was knocked down in CAL27 and HN30 cells, cell proliferation and colony formation ability was downregulated. Cell invasion ability was also suppressed. But cell apoptosis rate was induced reversely. In addition, the level of critical members in PI3K signaling pathway including PI3K, mTOR, Akt, and PDK-1 were significantly reduced after ANLN was knocked down in CAL27 cells. Conclusions: ANLN contributes to progression in oral cancer and affects activation of PI3K/mTOR signaling pathway. This study provides a new potential target for therapy and drug development in oral cancer.

Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

ANLN Promotes Carcinogenesis in Oral Cancer by Regulating PI3K/mTOR Signaling Pathway

Zhang

et al. 2020

Preprint

“…This data further supports that ANLN is associated with poor prognosis in cancer patients and enlarges the list of cancers affected by ANLN. Based on the public data, ANLN could promote cell proliferation and growth in cancer and increase the ability of cell migration and invasion [2][3][4][5][6][7]. Our data was consistent with the previous study and for rst time, we disclosed the secret of ANLN in oral cancer.…”

Section: Discussionsupporting

confidence: 90%

“…For example, overexpression of ANLN promoted cell metastasis in lung adenocarcinoma and patients with higher ANLN expression displayed much worse prognosis [3,4]. Overexpression of ANLN was found in pancreatic cancer but reduction of ANLN by microRNA inhibited cell aggressiveness ability [5,6]. In cervical cancer, bioinformatics analysis demonstrated that ANLN might be a candidate biomarker for evaluation of survival [7].…”

Section: Introductionmentioning

confidence: 99%

ANLN promotes carcinogenesis in oral cancer by regulating PI3K/mTOR signaling pathway

Zhang

et al. 2020

Preprint

Background: Oral cancer is a malignant disease threatening human’s life and severely reduces human’s life-quality. Gene ANLN was reported to promote progression in cancer. This study aims at investigating the role of ANLN and molecular mechanism in oral cancer. Methods: ANLN was down-regulated by RNAi technology. The effect of ANLN on cell behaviors including proliferation, cycle distribution, invasion, and apoptosis was detected. Western blotting analysis was used to disclose the mechanism of ANLN in oral cancer. Results: ANLN was shown to express significantly higher in tumor tissues compared to the normal control tissues based on TCGA data. Patients with higher expression of ANLN displayed worse survival rate. Then ANLN was shown to express abundantly in cancer cell lines CA127 and HN30. When ANLN was reduced in CA127 and HN30 cells, cell proliferation and colony formation ability was inhibited. Cell invasion ability was suppressed. But cell apoptosis was induced reversely. In addition, expression of critical molecules including PI3K, mTOR, Akt, and PDK-1 were reduced after ANLN knockdown in CA127 cells. Conclusions: ANLN contributes to the progression in oral cancer and regulates activation of PI3K/mTOR signaling pathway. This study will provide guidance and new drug target for oral cancer.

“…It regulates cell division and cell cycle (Wang et al, 2018). Anillin (ANLN) encodes an actin-binding protein that consists of 1125 amino acids and plays an important role in cytokinesis (Wang et al, 2019). Laminin γ2 (LAMC2), LAMB3 and LAMA3 constitutes the heterotrimeric glycoprotein laminin-332, then regulate the migration of epithelial cells and promote cancer invasion (Masuda et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Upregulation of desmoglein 2 and its clinical value in lung adenocarcinoma: a comprehensive analysis by multiple bioinformatics methods

Sun

Yang

2020

PeerJ

Background Desmoglein-2 (DSG2), a desmosomal adhesion molecule, is found to be closely related to tumorigenesis in recent years. However, the clinical value of DSG2 in lung adenocarcinoma remains unclear. Methods Real-time reverse transcription-quantitative polymerase chain reaction (qRT-PCR) was utilized to detect the expression of DSG2 in 40 paired lung adenocarcinoma tissues and corresponding non-cancerous tissues. Data from The Cancer Genome Atlas (TCGA) and Oncomine datasets were also downloaded and analyzed. The correlation between DSG2 and clinicopathological features was investigated. The expression of DSG2 protein by immunohistochemical was also detected from tissue microarray and the Human Protein Atlas database. Integrated meta-analysis combining the three sources (qRT-PCR data, TCGA data and Oncomine datasets) was performed to evaluate the clinical value of DSG2. Univariate and multivariate Cox regression analyses were used to explore the prognostic value of DSG2. Then, co-expressed genes were calculated by Pearson correlation analysis. Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were used to investigate the underlying molecular mechanism. The expression level in lung adenocarcinoma and prognostic significance of the top ten co-expressed genes were searched from Gene Expression Profiling Interactive Analysis (GEPIA) online database. Results DSG2 was highly expressed in lung adenocarcinoma tissues based on qRT-PCR, TCGA and Oncomine datasets. The protein expression of DSG2 was also higher in lung adenocarcinoma. According to qRT-PCR and TCGA, high DSG2 expression was positively associated with tumor size (p = 0.027, p = 0.001), lymph node metastasis (p = 0.014, p < 0.001) and TNM stage (p = 0.023, p < 0.001). The combined standard mean difference values of DSG2 expression based on the three sources were 1.30 (95% confidence interval (CI): 1.08–1.52) using random effect model. The sensitivity and specificity were 0.73 (95% CI [0.69–0.76]) and 0.96 (95% CI [0.89–0.98]). The area under the curve based on summarized receiver operating characteristic (SROC) curve was 0.79 (95% CI [0.75–0.82]). Survival analysis revealed that high DSG2 expression was associated with a short overall survival (hazard ratio [HR] = 1.638; 95% CI [1.214–2.209], p = 0.001) and poor progression-free survival (HR = 1.475; 95% CI [1.102–1.974], p < 0.001). A total of 215 co-expressed genes were identified. According to GO and KEGG analyses, these co-expressed genes may be involved in “cell division”, “cytosol”, “ATP binding” and “cell cycle”. Based on GEPIA database, seven of the top ten co-expressed genes were highly expressed in lung adenocarcinoma (DSC2, SLC2A1, ARNTL2, ERO1L, ECT2, ANLN and LAMC2). High expression of these genes had shorter overall survival. Conclusions The expression of DSG2 is related to the tumor size, lymph node metastasis and TNM stage. Also, DSG2 predicts poor prognosis in lung adenocarcinoma.