ArticleCancer biomarkers : section A of Disease markers2019
Downregulation of GATS gene inhibits proliferation, clonogenicity and migration in triple negative breast cancer cells MDA-MB-231 by cell autophagy.
Article in Cancer biomarkers : section A of Disease markers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 4 citations in OpenAlex.
- Reannotation of Public Transcriptomic Data Identifies Candidate lncRNAs and Putative Regulatory Networks in Rhabdomyosarcoma.Biomedicines · 2026Article
- Multi-transcriptomics predicts clinical outcome in systemically untreated breast cancer patients with extensive follow-up.Breast cancer research : BCR · 2025Article
- HTB50-2 Inhibits Growth and Migration of Triple-negative Breast Cancer via FOSL2/FOXC1 Signaling Axis and Subsequent Ferroptosis.Current medicinal chemistry · 2025Article
- The roles of CPSF6 in proliferation, apoptosis and tumorigenicity of lung adenocarcinoma.Aging · 2022Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The triple negative breast cancer (TNBC) accounts for 15% to 20% of the total number of breast cancer diagnosed. A number of clinical studies have shown that TNBC has a high risk of early recurrence and distant metastasis, and a low rate of disease free survival and total survival. The premise of TNBC deterioration was abnormal proliferation and migration of tumor cells, and this study firstly showed that GATS gene could promote proliferation of MDA-MB-231 breast cancer cells. Through lentiviral expression system, the GATS gene was konckdown by shGATS lentivirus infection in the MDA-MB-231 cells, and the result indicated it could remarkably decrease the ability of cell proliferation and migration. Real-time PCR, western blot and immunofluorescence experiments showed the expressions of protein LC3, and p-Akt in shGATS cell group were lower than the shCtrl group. Therefore, we suggest the GATS could promote the MDA-MB-231 cell proliferation, migration and clonogenicity through cell autophagy by the PI3K/Akt pathway, which paved the way for further study the function of GATS in TNBC, and GATS may potentially be a target for gene therapy against triple negative breast cancer.
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