Evidence map›Paper›PMID 29288363›Full record

ArticleJournal of cancer research and clinical oncology2018

Targeting LC3 and Beclin-1 autophagy genes suppresses proliferation, survival, migration and invasion by inhibition of Cyclin-D1 and uPAR/Integrin β1/ Src signaling in triple negative breast cancer cells.

Zuhal Hamurcu, Nesrin Delibaşı, Seda Geçene, Elif Funda Şener, Hamiyet Dönmez-Altuntaş, Yusuf Özkul, Halit Canatan, Bulent Ozpolat

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
6.4field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

68 citing papers in PubMed, 116 citations in OpenAlex.

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  15. The IPBiochimica et biophysica acta. Molecular basis of disease · 2025
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8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Zuhal HamurcuDepartment of Medical Biology, Faculty of Medicine, Erciyes University, Kayseri, Turkey.
Nesrin DelibaşıDepartment of Medical Biology, Faculty of Medicine, Erciyes University, Kayseri, Turkey.
Seda GeçeneDepartment of Medical Biology, Faculty of Medicine, Erciyes University, Kayseri, Turkey.
Elif Funda ŞenerDepartment of Medical Biology, Faculty of Medicine, Erciyes University, Kayseri, Turkey.
Hamiyet Dönmez-AltuntaşDepartment of Medical Biology, Faculty of Medicine, Erciyes University, Kayseri, Turkey.
Yusuf ÖzkulDepartment of Medical Biology, Faculty of Medicine, Erciyes University, Kayseri, Turkey.
Halit CanatanDepartment of Medical Biology, Faculty of Medicine, Erciyes University, Kayseri, Turkey.
Bulent OzpolatDepartment of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 422, Houston, TX, 77030, USA. bozpolat@mdanderson.org.ORCID http://orcid.org/0000-0002-0711-4014
Erciyes University · TRThe University of Texas MD Anderson Cancer Center · US

Funding

The Scientific and Technological Research Council -TÜBİTAK- research grant 214S204
6 · The paper itself

Abstract

Autophagy is a catabolic process for degrading dysfunctional proteins and organelles, and closely associated with cancer cell survival under therapeutic, metabolic stress, hypoxia, starvation and lack of growth factors, contributing to resistance to therapies. However, the role of autophagy in breast cancer cells is not well understood. In the present study, we investigated the role of autophagy in highly aggressive and metastatic triple negative breast cancer (TNBC) and non-metastatic breast cancer cells and demonstrated that the knockdown of autophagy-related genes (LC3 and Beclin-1) inhibited autophagy and significantly suppressed cell proliferation, colony formation, migration/invasion and induced apoptosis in MDA-MB-231 and BT-549 TNBC cells. Knockdown of LC3 and Beclin-1 led to inhibition of multiple proto-oncogenic signaling pathways, including cyclin D1, uPAR/integrin-β1/Src, and PARP1. In conclusion, our study suggests that LC3 and Beclin-1 are required for cell proliferation, survival, migration and invasion, and may contribute to tumor growth and progression of highly aggressive and metastatic TNBC cells and therapeutic targeting of autophagy genes may be a potential therapeutic strategy for TNBC in breast cancer.

Indexed as

AutophagyBeclin-1Cell Line, TumorCell MovementCell ProliferationCell SurvivalCyclin D1FemaleGene Expression Regulation, NeoplasticHumansIntegrin beta1MCF-7 CellsMicrotubule-Associated ProteinsMolecular Targeted TherapyReceptors, Urokinase Plasminogen ActivatorRNA, Small InterferingBeclin-1CCND1 protein, humanCyclin D1Integrin beta1MAP1LC3A protein, humanMicrotubule-Associated ProteinsReceptors, Urokinase Plasminogen ActivatorRNA, Small Interferingsrc-Family KinasesAutophagyBeclin-1 siRNABreast cancerInvasionLC3MetastasisMigrationProliferationTNBCTreatmentTriple-negative breast cancer

Identifiers

PMID29288363
PMCPMC11813384
OpenAlexW2778789248

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.