Proteomics

Dataset Information

0

The quantitative proteomics analysis of TGF-β induced EMT in A549 cells and TNS-overexpressing A549 cells


ABSTRACT: Metastasis is the primary cause of mortality in lung cancer patients, with the epithelial-mesenchymal transition (EMT) process conferring increased metastatic potential to carcinoma cells. While emerging evidence suggests that TNS1 contributes to carcinoma metastasis, it remains unclear the role of TNS1 in EMT. In this study, we reveal TNS1 as an indispensable factor in TGF-β and hypoxia mediated EMT process. Elevated TNS1 protein levels are closely correlated with a worse prognosis in lung cancer patients. TNS1 is also found to potently promote EMT process and tumor metastasis in vitro and in vivo. Mechanistically, TNS1 expression is mediated by the transcription factor SMAD3 in TGF-β signaling. Moreover, TNS1 interacts with and modulates ZEB1 expression, preventing ZEB1 ubiquitination degradation. Therefore, our study reveals the role of TNS1 in the EMT process and suggests that TNS1 promises to a candidate for targeted cancer therapy.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Lung Cancer

SUBMITTER: Tingting Zhang  

LAB HEAD: Yong Peng

PROVIDER: PXD057161 | Pride | 2025-12-08

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
TGF_beta_TMT1.raw Raw
TGF_beta_TMT10.raw Raw
TGF_beta_TMT11.raw Raw
TGF_beta_TMT12.raw Raw
TGF_beta_TMT2.raw Raw
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Publications

A positive feedback loop between TNS1 and ZEB1 promotes TGFβ-induced epithelial-to-mesenchymal transition in lung cancer.

Zhang Tingting T   Li Zhang Z   Ming Yue Y   Li Jiao J   Ye Zixia Z   Luo Dongdong D   Wang Rui R   Yang Yang Y   Yang Xiaojuan X   Peng Yong Y  

Communications biology 20251126 1


Epithelial-mesenchymal transition (EMT) plays a pivotal role in tumor metastasis initiation. Although emerging evidence suggests that Tensin-1 (TNS1) contributes to tumor metastasis, its precise function in EMT during lung cancer progression and the underlying mechanisms remain unclear. Here, we identify that TNS1 is upregulated in a TGFβ-induced EMT cell model. Functional studies demonstrate that TNS1 knockdown significantly attenuates both TGFβ- and hypoxia-induced EMT, highlighting its critic  ...[more]

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