ArticleInternational journal of clinical and experimental medicine2015
Autophagic regulation of cell growth by altered expression of Beclin 1 in triple-negative breast cancer.
Article in International journal of clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 36 citations in OpenAlex.
- Stromal hypoxia and autophagy signatures as indicators of pathologic response in triple-negative breast cancer.BMC cancer · 2026Article
- Global research status and frontiers on autophagy in triple negative breast cancer (TNBC): a comprehensive bibliometric and visualized analysis.Discover oncology · 2025Article
- CAFs exosomal circFOXO1 promotes TNBC autophagy and radioresistance via miR-27a-3p/BNIP3 axis.Scientific reports · 2025Article
- Food Waste to Wellness: A Grape Pomace Blend in Gastric Cancer Prevention.Food science & nutrition · 2025Article
- The role of autophagy in cancer: from molecular mechanism to therapeutic window.Frontiers in immunology · 2025Review
- Protective effects of adipose-derived stem cells against testicular injury induced after ischemia-reperfusion by regulating autophagy.Histochemistry and cell biology · 2024Article
- Cell Death: Mechanisms and Potential Targets in Breast Cancer Therapy.International journal of molecular sciences · 2024Review
- BECN1 mRNA expression in breast cancer tissue; significant correlation to tumor grade.Molecular genetics and genomics : MGG · 2024Article
- ANXA2 (annexin A2) is crucial to ATG7-mediated autophagy, leading to tumor aggressiveness in triple-negative breast cancer cells.Autophagy · 2024Article
- Advances in the study of autophagy in breast cancer.Breast cancer (Tokyo, Japan) · 2024Review
- Roles of Rictor alterations in gastrointestinal tumors (Review).Oncology reports · 2024Article
- Hypoxia-induced autophagy in triple negative breast cancer: association with prognostic variables, patients' survival and response to neoadjuvant chemotherapy.Virchows Archiv : an international journal of pathology · 2023Article
- Cadmium-induced impairment of spermatozoa development by reducing exosomal-MVBs secretion: a novel pathway.Aging · 2023Article
- Review
- β-Caryophyllene Counteracts Chemoresistance Induced by Cigarette Smoke in Triple-Negative Breast Cancer MDA-MB-468 Cells.Biomedicines · 2022Article
- Etanercept Mitigates Cadmium Chloride-induced Testicular Damage in Rats "An Insight into Autophagy, Apoptosis, Oxidative Stress and Inflammation".Environmental science and pollution research international · 2022Article
- miR-214 Modulates the Growth and Migration of Oral Cancer before and after Chemotherapy through Mediating ULK1.Journal of immunology research · 2022Article
- A curcumin analog CA-5f inhibits urokinase-type plasminogen activator and invasive phenotype of triple-negative breast cancer cells.Toxicological research · 2022Article
- Review
- The Complex Interplay of Inflammation, Metabolism, Epigenetics, and Sex in Calcific Disease of the Aortic Valve.Frontiers in cardiovascular medicine · 2021Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Beclin 1 is a promoter gene for autophagy as well as a key factor for regulating tumor cell growth and death. Allelic deletion of Beclin 1 has been observed in certain triple-negative breat cancer (TNBC) cells, and it might be associated with increased proliferation and invasion in TNBC cells. In this study we investigated the relationship between Beclin 1 expression and prognosis for TNBC patients, as well as the influence on cell growth by Beclin 1 overexpression in different cultural conditions. Beclin 1 expression in TNBC tissues was measured by immunohistochemical staining and correlated with clinicopathologic parameters for TNBC patients. The plasmid of pDS-RED-C1-Beclin 1 was transfected to BT-549 and MDA-MB-231 cells and autophagy, proliferation, apoptosis, cell cycle and Epithelial-mesenchymal transition (EMT) process were measured. Results indicated that high level of Beclin 1 expression was correlated with more lymph nodes and distant metastasis but unrelated to survival rates in 5 years for TNBC patients. In vitro, overexpression of Beclin 1 improved cellular autophagy in both BT-549 and MDA-MB-231 cells, inhibited cell proliferation at normal cultural condition and increased cell survival in starvation, hypoxia or with doxorubicin stimulation. Besides, Beclin 1 overexpression decreased cell apoptosis, induced cells to be in G0/G1 phase and promoted EMT process through Wnt/β-catenin pathway in starvation. Thus, Beclin 1 overexpression plays a double role in BT-549 and MDA-MB-231 cell growth by elevating the capability of autophagy. These findings might be useful for searching a proper method for clinical therapy of TNBC from the aspect of autophagy in future.
Indexed as
Identifiers
26221242PMC4509187W2398137309What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.