Evidence map›Paper›PMID 33414642›Full record

ArticleOncoTargets and therapy2020

BCL-2 Inhibitor Venetoclax Induces Autophagy-Associated Cell Death, Cell Cycle Arrest, and Apoptosis in Human Breast Cancer Cells.

Ali Alhoshani, Fahad O Alatawi, Fawaz E Al-Anazi, Ibraheem M Attafi, Asad Zeidan, Abdelali Agouni, Heba M El Gamal, Licia S Shamoon, Sarah Khalaf, Hesham M Korashy

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

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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

10 authors at 3 institutions in 2 countries.

Ali AlhoshaniDepartment of Pharmacology & Toxicology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.ORCID 0000-0002-3450-283X
Fahad O AlatawiDepartment of Pharmacology & Toxicology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.ORCID 0000-0002-3230-2279
Fawaz E Al-AnaziDepartment of Pharmacology & Toxicology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia.ORCID 0000-0002-8353-2066
Ibraheem M AttafiPoison Control & Medical Forensic Chemistry Center, Jazan Health Affairs, Jazan, Saudi Arabia.ORCID 0000-0001-5801-8500
Asad ZeidanDepartment of Biomedical Sciences, College of Medicine, QU Health, Qatar University, Doha, Qatar.
Abdelali AgouniDepartment of Pharmaceutical Sciences, College of Pharmacy, QU Health, Qatar University, Doha, Qatar.ORCID 0000-0002-8363-1582
Heba M El GamalDepartment of Pharmaceutical Sciences, College of Pharmacy, QU Health, Qatar University, Doha, Qatar.
Licia S ShamoonDepartment of Pharmaceutical Sciences, College of Pharmacy, QU Health, Qatar University, Doha, Qatar.
Sarah KhalafDepartment of Pharmaceutical Sciences, College of Pharmacy, QU Health, Qatar University, Doha, Qatar.
Hesham M KorashyDepartment of Pharmaceutical Sciences, College of Pharmacy, QU Health, Qatar University, Doha, Qatar.ORCID 0000-0002-5745-9643
Qatar University · QAKing Saud University · SAJazan University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionVenetoclax (VCX) is a selective BCL-2 inhibitor approved for the treatment of leukemia and lymphoma. However, the mechanisms of anti-cancer effect of VCX either as a monotherapy or in combination with other chemotherapeutic agents against breast cancer need investigation.

methodsBreast cancer cell lines with different molecular subtypes (MDA-MB-231, MCF-7, and SKBR-3) were treated with different concentrations of VCX for indicated time points. The expression of cell proliferative, apoptotic, and autophagy genes was determined by qRT-PCR and Western blot analyses. In addition, the percentage of MDA-MB-231 cells underwent apoptosis, expressed higher oxidative stress levels, and the changes in the cell cycle phases were determined by flow cytometry.

resultsTreatment of human breast cancer cells with increasing concentrations of VCX caused a significant decrease in cells growth and proliferation. This effect was associated with a significant increase in the percentage of apoptotic MDA-MB-231 cells and in the expression of the apoptotic genes, caspase 3, caspase 7, and BAX, with inhibition of anti-apoptotic gene, BCL-2 levels. Induction of apoptosis by VCX treatment induced cell cycle arrest at G0/G1 phase with inhibition of cell proliferator genes, cyclin D1 and E2F1. Furthermore, VCX treatment increased the formation of reactive oxygen species and the expression level of autophagy markers, Beclin 1 and LC3-II. Importantly, these cellular changes by VCX increased the chemo-sensitivity of MDA-MB-231 cells to doxorubicin. DISCUSSION: The present study explores the molecular mechanisms of VCX-mediated inhibitory effects on the growth and proliferation of TNBC MDA-MB-231 cells through the induction of apoptosis, cell cycle arrest, and autophagy. The study also explores the role of BCL-2 as a novel targeted therapy for breast cancer.

Indexed as

apoptosisautophagyBCL-2breast cancercell cycleMDA-MB-231 cellsvenetoclax

Identifiers

PMID33414642
PMCPMC7783200
OpenAlexW3115208379

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.