scholarly journals SOX5 predicts poor prognosis in lung adenocarcinoma and promotes tumor metastasis through epithelial-mesenchymal transition

Oncotarget ◽  
2017 ◽  
Vol 9 (13) ◽  
pp. 10891-10904 ◽  
Author(s):  
Xin Chen ◽  
Yufei Fu ◽  
Hongfei Xu ◽  
Peng Teng ◽  
Qiong Xie ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Poor Prognosis ◽  
Tumor Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition

scholarly journals RUFY3 Predicts Poor Prognosis and Promotes Metastasis through Epithelial-mesenchymal Transition in Lung Adenocarcinoma

2019 ◽  
Vol 10 (25) ◽  
pp. 6278-6285 ◽  
Author(s):  
Wanfu Men ◽  
Wenya Li ◽  
Yu Li ◽  
Jungang Zhao ◽  
Xiaohan Qu ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition

scholarly journals CHIP-mediated CIB1 ubiquitination regulated epithelial–mesenchymal transition and tumor metastasis in lung adenocarcinoma

2020 ◽  
Author(s):  
Yuanqi Liu ◽  
Yanwu Zhou ◽  
Pengfei Zhang ◽  
Xizhe Li ◽  
Chaojun Duan ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Tumor Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Clinicopathological Characteristics ◽  
Interacting Protein ◽  
Mesenchymal Transition ◽  
Normal Tissues ◽  
Ubiquitin E3 Ligase ◽  
And Migration

Abstract CIB1 is a homolog of calmodulin that regulates cell adhesion, migration, and differentiation. It has been considered as an oncogene in many tumor cells; however, its role in lung adenocarcinoma (LAC) has not been studied. In this study, the expression levels of CIB1 in LAC tissues and adjacent normal tissues were examined by immunohistochemistry, and the relationship between CIB1 expression and patient clinicopathological characteristics was analyzed. The effects of CIB1 on epithelial–mesenchymal transition (EMT), migration, and metastasis of LAC cells were determined in vitro and vivo. Proteins interacting with CIB1 were identified using electrospray mass spectrometry (LS-MS), and CHIP was selected in the following assays. Carboxyl-terminus of Hsp70-interacting protein (CHIP) is a ubiquitin E3 ligase. We show that CHIP can degrade CIB1 via promoting polyubiquitination of CIB1 and its subsequent proteasomal degradation. Besides, lysine residue 10 and 65 of CIB1 is the ubiquitinated site of CIB1. Furthermore, CHIP-mediated CIB1 downregulation is critical for the suppression of metastasis and migration of LAC. These results indicated that CHIP-mediated CIB1 ubiquitination could regulate epithelial–mesenchymal and tumor metastasis in LAC.

scholarly journals HSD17B6 downregulation predicts poor prognosis and drives tumor progression via activating Akt signaling pathway in lung adenocarcinoma

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Tian Tian ◽  
Fu Hong ◽  
Zhiwen Wang ◽  
Jiaru Hu ◽  
Ni Chen ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Lung Adenocarcinoma ◽  
Poor Prognosis ◽  
Epithelial Mesenchymal Transition ◽  
Tumor Grade ◽  
Tumor Stage ◽  
Advanced Tumor Stage ◽  
Large Tumor ◽  
Mesenchymal Transition ◽  
Advanced Tumor

AbstractLung adenocarcinoma is one of the most frequent tumor subtypes, involving changes in a variety of oncogenes and tumor suppressor genes. Hydroxysteroid 17-Beta Dehydrogenase 6 (HSD17B6) could synthetize dihydrotestosterone, abnormal levels of which are associated with progression of multiple tumors. Previously, we showed that HSD17B6 inhibits malignant progression of hepatocellular carcinoma. However, the mechanisms underlying inhibiting tumor development by HSD17B6 are not clear. Moreover, its role in lung adenocarcinoma (LUAD) is yet unknown. Here, we investigated its expression profile and biological functions in LUAD. Analysis of data from the LUAD datasets of TCGA, CPTAC, Oncomine, and GEO revealed that HSD17B6 mRNA and protein expression was frequently lower in LUAD than in non-neoplastic lung tissues, and its low expression correlated significantly with advanced tumor stage, large tumor size, poor tumor differentiation, high tumor grade, smoking, and poor prognosis in LUAD. In addition, its expression was negatively regulated by miR-31-5p in LUAD. HSD17B6 suppressed LUAD cell proliferation, migration, invasion, epithelial–mesenchymal transition (EMT), and radioresistance. Furthermore, HSD17B6 overexpression in LUAD cell lines enhanced PTEN expression and inhibited AKT phosphorylation, inactivating downstream oncogenes like GSK3β, β-catenin, and Cyclin-D independent of dihydrotestosterone, revealing an underlying antitumor mechanism of HSD17B6 in LUAD. Our findings indicate that HSD17B6 may function as a tumor suppressor in LUAD and could be a promising prognostic indicator for LUAD patients, especially for those receiving radiotherapy.

scholarly journals CXCR6 predicts poor prognosis in gastric cancer and promotes tumor metastasis through epithelial-mesenchymal transition

2017 ◽  
Vol 37 (6) ◽  
pp. 3279-3286 ◽  
Author(s):  
Jie-Jie Jin ◽  
Fa-Xiang Dai ◽  
Zi-Wen Long ◽  
Hong Cai ◽  
Xiao-Wen Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Poor Prognosis ◽  
Tumor Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition

scholarly journals DCBLD2 Mediates Epithelial-Mesenchymal Transition-Induced Metastasis by Cisplatin in Lung Adenocarcinoma

Cancers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1403
Author(s):  
Xiaosu Chen ◽  
Yajing Lv ◽  
Kejia Xu ◽  
Xiaoshuang Wang ◽  
Yujia Zhao ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Tumor Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Bioinformatic Analysis ◽  
Critical Issue ◽  
Chemotherapeutic Agents ◽  
Clinical Practices ◽  
Mesenchymal Transition

Growing evidence suggests that cisplatin and other chemotherapeutic agents promote tumor metastasis while inhibiting tumor growth, which is a critical issue for certain patients in clinical practices. However, the role of chemotherapeutics in promoting tumor metastasis and the molecular mechanism involved are unclear. Here, we investigated the roles of cisplatin in promoting tumor metastasis in lung adenocarcinoma (LUAD). We demonstrated that cisplatin promoted epithelial-mesenchymal transition (EMT), cell motility, and metastasis in vitro and in vivo. The bioinformatic analysis and molecular biology approaches also indicated that DCBLD2 (Discoidin, CUB and LCCL domain containing 2) is a key gene that mediates cisplatin-induced metastasis. DCBLD2 stabilizes β-catenin by phosphorylating GSK3β and transporting accumulated β-catenin to the nucleus to promote the expression of EMT-related transcriptional factors (TFs), ultimately resulting in tumor metastasis. We also identified that cisplatin enhanced DCBLD2 expression by phosphorylating ERK and hence the AP-1-driven transcription of DCBLD2. Furthermore, DCBLD2-specific siRNAs encapsulated by nanocarriers prominently inhibit cisplatin-induced metastasis in vivo. Therefore, DCBLD2 plays a key role in cisplatin-induced metastasis in LUAD and is a potential target for preventing chemotherapy-induced metastasis in vivo.

scholarly journals High expression of TRIM29 (ATDC) contributes to poor prognosis and tumor metastasis by inducing epithelial-mesenchymal transition in osteosarcoma

2017 ◽  
Vol 38 (3) ◽  
pp. 1645-1654 ◽  
Author(s):  
Si-Xiang Zeng ◽  
Qing-Chun Cai ◽  
Chi-Hua Guo ◽  
Li-Qiang Zhi ◽  
Xing Dai ◽  
...  
Keyword(s):  
Poor Prognosis ◽  
Tumor Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
High Expression ◽  
Mesenchymal Transition

scholarly journals Expression of OPN3 in lung adenocarcinoma promotes epithelial‐mesenchymal transition and tumor metastasis

2019 ◽  
Vol 11 (2) ◽  
pp. 286-294 ◽  
Author(s):  
Chao Xu ◽  
Ruixia Wang ◽  
Yanfang Yang ◽  
Tongyi Xu ◽  
Yan Li ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Tumor Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition
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