Evidence map›Paper›PMID 41212350›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2026

Suppression of NGALR impedes TNBC cell survival, proliferation, invasion, and migration through Akt/mTOR and JAK/STAT3 pathway inhibition.

Krishan Kumar Thakur, Choudhary Harsha, Bethsebie L Sailo, Arunachalam Chinnathambi, Sulaiman Ali Alharbi, Mangala Hegde, Javadi Monisha, Zhaowu Ma, Ajaikumar B Kunnumakkara

Abstract read
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In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

9 authors.

Krishan Kumar ThakurCancer Biology Laboratory, Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati, Guwahati, 781 039, Assam, India.
Choudhary HarshaCancer Biology Laboratory, Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati, Guwahati, 781 039, Assam, India.
Bethsebie L SailoCancer Biology Laboratory, Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati, Guwahati, 781 039, Assam, India.
Arunachalam ChinnathambiDepartment of Botany and Microbiology, College of Science, King Saud University, PO Box 2455, Riyadh, 11451, Saudi Arabia.
Sulaiman Ali AlharbiDepartment of Botany and Microbiology, College of Science, King Saud University, PO Box 2455, Riyadh, 11451, Saudi Arabia.
Mangala HegdeCancer Biology Laboratory, Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati, Guwahati, 781 039, Assam, India.
Javadi MonishaCancer Biology Laboratory, Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati, Guwahati, 781 039, Assam, India.
Zhaowu MaSchool of Basic Medicine, Health Science Center, Yangtze University, 1 Nanhuan Road, Jingzhou, 434023, Hubei, China. mazw@yangtzeu.edu.cn.
Ajaikumar B KunnumakkaraCancer Biology Laboratory, Department of Biosciences and Bioengineering, Indian Institute of Technology Guwahati, Guwahati, 781 039, Assam, India. kunnumakkara@iitg.ac.in.ORCID http://orcid.org/0000-0001-9121-6816

Funding

Indian Institute of Technology Guwahati IITG/BSBE/ABK/PDF-01
6 · The paper itself

Abstract

purposeTriple-negative breast cancer (TNBC) represents an aggressive breast cancer subtype lacking estrogen, progesterone, and HER2 receptors, thereby limiting targeted therapeutic options. The present study aimed to elucidate the functional significance of neutrophil gelatinase-associated lipocalin receptor (NGALR) in TNBC progression and evaluate its potential as a therapeutic target.

methodsExpression levels of NGALR were analyzed in TNBC cell lines and tissue samples. Functional assays were performed following siRNA-mediated silencing of NGALR to assess effects on cell proliferation, survival, migration, and invasion. Changes in cell cycle distribution, autophagy induction, and expression of associated regulatory proteins were examined using flow cytometry and immunoblotting. The modulation of key signaling pathways, including Akt/mTOR and JAK/STAT3, was also investigated.

resultsNGALR was markedly upregulated in TNBC cells and tissues compared with controls. NGALR knockdown significantly reduced cell proliferation and survival, induced S-phase arrest, and enhanced autophagic activity. Silencing NGALR decreased the expression of Bcl-2, Cox-2, Cyclin A2, and survivin while increasing p21 levels. Additionally, NGALR suppression diminished migratory and invasive capabilities, accompanied by reduced expression of N-cadherin, Vimentin, Snail, Twist-1, VEGF-A, and CXCR-4, and enhanced E-cadherin levels. Inhibition of NGALR also downregulated the Akt/mTOR and JAK/STAT3 signaling cascades, both integral to TNBC progression.

conclusionsThe study demonstrates that NGALR promotes TNBC cell growth, invasion, and survival through modulation of cell cycle, autophagy, and oncogenic signaling pathways. NGALR represents a promising therapeutic target warranting further preclinical and clinical validation.

Indexed as

Triple Negative Breast NeoplasmsAutophagyCell Line, TumorCell MovementCell ProliferationCell SurvivalFemaleHumansJanus KinasesNeoplasm InvasivenessProto-Oncogene Proteins c-aktSignal TransductionSTAT3 Transcription FactorTOR Serine-Threonine KinasesJanus KinasesMTOR protein, humanProto-Oncogene Proteins c-aktSTAT3 protein, humanSTAT3 Transcription FactorTOR Serine-Threonine KinasesKnockdownNGALRProliferationSurvivalTNBC

Identifiers

PMID41212350

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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.