Overexpression of TMEM158 contributes to ovarian carcinogenesis

Cheng, Zhongping; Guo, Jing; Chen, Li; Luo, Ning; Yang, Wei; Qu, Xun

doi:10.1186/s13046-015-0193-y

Cited by 44 publications

(49 citation statements)

References 28 publications

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“…By interaction with Smad complex (Smad‐mediated canonical or noncanonical signaling pathway), several transcription factors are initiated so as to result in EMT (Giannelli et al, ; Moustakas & Heldin, ; Yu et al, ). Cheng et al () reported that TMEM158 promoted the migration and adhesion of ovarian cancer cells by upregulation of TGFβ1, BMP4, ICAM1, and IVCAM1. According to the TCGA data set, interestingly, a significant positive association within the expression profile of TMEM158 and TGFβ1 was really existed in PC samples.…”

Section: Discussionmentioning

confidence: 99%

TMEM158 promotes pancreatic cancer aggressiveness by activation of TGFβ1 and PI3K/AKT signaling pathway

Yao

Ding

et al. 2019

Journal Cellular Physiology

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Pancreatic cancer (PC) is one of the most deadly digestive cancers world-wide, with a dismal five-year survival rate of <8%. Upregulation of transmembrane protein 158 (TMEM158) is known to facilitate the progression of several carcinomas. However, little is known concerning the potential roles of TMEM158 in PC. Herein, we first found that TMEM158 was significantly upregulated in PC samples as well as PC cell lines. The overexpression of TMEM158 was significantly correlated with advanced clinicopathologic features (including tumor size, TNM stage, and blood vessel invasion) and poorer prognosis of patients with PC in clinic. Evidenced based on a series of loss-and gain-of-function assays uncovered that TMEM158 enhanced PC cell proliferation, migration, and invasion by stimulating the progression of cell cycle, epithelial-mesenchymal transition, and MMP-2/9 production. Furthermore, mechanism-related investigations disclosed that activation of TGFβ1 and PI3K/AKT signal might be responsible for TMEM158-triggered PC aggressiveness. Collectively, TMEM158 was upregulated in PC and promoted PC cell proliferation, migration, and invasion through the activation of TGFβ1 and PI3K/AKT signaling pathways, highlighting its potential as a tumor promoter and a therapeutic target for PC. K E Y W O R D Scarcinogenesis, pancreatic cancer, PI3K/AKT, TGFβ1, TMEM158

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Section: Discussionmentioning

confidence: 99%

TMEM158 promotes pancreatic cancer aggressiveness by activation of TGFβ1 and PI3K/AKT signaling pathway

Yao

Ding

et al. 2019

Journal Cellular Physiology

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“…Ovarian cancer is the leading cause of cancer-associated mortality in gynecology worldwide. MEOC is successfully treated in <40% of women, due to the lack of effective screening strategies and the non-specific nature of early signs and symptoms associated with this disease, resulting in an advanced stage diagnosis for the majority of patients (15,16). Tumor recurrence and metastasis are considered the major reasons for poor clinical outcomes and mortality.…”

Section: Discussionmentioning

confidence: 99%

Association between the HMGB1/TLR4 signaling pathway and the clinicopathological features of ovarian cancer

Jiang

et al. 2018

Mol Med Report

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In the present study, the expression levels of high‑mobility group protein B1 (HMGB1), Toll‑like receptor 4 (TLR4), nuclear factor (NF)‑κB and tumor necrosis factor (TNF)‑α in malignant epithelial ovarian cancer (MEOC) were investigated in regards to several clinicopathological characteristics. A total of 20 patients with MEOC who underwent surgery were recruited in the present study. The mRNA and protein expression of HMGB1, TLR4, NF‑κB and TNF‑α was determined in patients with MEOC and compared with expression levels in 20 patients diagnosed with benign ovarian cysts (BOC). It was demonstrated that the mRNA and protein expression of HMGB1, TLR4, NF‑κB and TNF‑α in MEOC was significantly increased, compared with the BOC group (P<0.01). The gene and protein expression of HMGB1, TLR4, NF‑κB and TNF‑α was significantly increased in the advanced tumor stage and poorly differentiated group (P<0.01). The present study suggested that the HMGB1/TLR4 signaling pathway was overactive in MEOC, and was associated with MEOC tumor cell proliferation, invasion and metastasis. Furthermore, this may have been mediated via NF‑κB signaling.

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“…8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18 However, little is known regarding the association between TMEMs and osteosarcoma. TMEM119, a member of the transmembrane protein family and also known as osteoblast induction factor (Obif), is O -glycosylated at its N-terminal region.…”

Section: Introductionmentioning

confidence: 99%

Upregulation and biological function of transmembrane protein 119 in osteosarcoma

et al. 2017

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Osteosarcoma is suggested to be caused by genetic and molecular alterations that disrupt osteoblast differentiation. Recent studies have reported that transmembrane protein 119 (TMEM119) contributes to osteoblast differentiation and bone development. However, the level of TMEM119 expression and its roles in osteosarcoma have not yet been elucidated. In the present study, TMEM119 mRNA and protein expression was found to be up-regulated in osteosarcoma compared with normal bone cyst tissues. The level of TMEM119 protein expression was strongly associated with tumor size, clinical stage, distant metastasis and overall survival time. Moreover, gene set enrichment analysis (GSEA) of the Gene Expression Omnibus (GEO) GSE42352 dataset revealed TMEM119 expression in osteosarcoma tissues to be positively correlated with cell cycle, apoptosis, metastasis and TGF-β signaling. We then knocked down TMEM119 expression in U2OS and MG63 cells using small interfering RNA, which revealed that downregulation of TMEM119 could inhibit the proliferation of osteosarcoma cells by inducing cell cycle arrest in G0/G1 phase and apoptosis. We also found that TMEM119 knockdown significantly inhibited cell migration and invasion, and decreased the expression of TGF-β pathway-related factors (BMP2, BMP7 and TGF-β). TGF-β application rescued the inhibitory effects of TMEM119 knockdown on osteosarcoma cell migration and invasion. Further in vitro experiments with a TGF-β inhibitor (SB431542) or BMP inhibitor (dorsomorphin) suggested that TMEM119 significantly promotes cell migration and invasion, partly through TGF-β/BMP signaling. In conclusion, our data support the notion that TMEM119 contributes to the proliferation, migration and invasion of osteosarcoma cells, and functions as an oncogene in osteosarcoma.

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Overexpression of TMEM158 contributes to ovarian carcinogenesis

Cited by 44 publications

References 28 publications

TMEM158 promotes pancreatic cancer aggressiveness by activation of TGFβ1 and PI3K/AKT signaling pathway

TMEM158 promotes pancreatic cancer aggressiveness by activation of TGFβ1 and PI3K/AKT signaling pathway

Association between the HMGB1/TLR4 signaling pathway and the clinicopathological features of ovarian cancer

Upregulation and biological function of transmembrane protein 119 in osteosarcoma

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