Evidence map›Paper›PMID 35699794›Full record

ArticleCellular and molecular life sciences : CMLS2022

Overexpression of laminin-5 gamma-2 promotes tumorigenesis of pancreatic ductal adenocarcinoma through EGFR/ERK1/2/AKT/mTOR cascade.

Anuradha Kirtonia, Amit Kumar Pandey, Balaji Ramachandran, Durga Prasad Mishra, David W Dawson, Gautam Sethi, Trivadi S Ganesan, H Phillip Koeffler, Manoj Garg

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
7.3field-weighted citation impact, top 2% 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

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

  1. Pooled it
  2. S100A10 promotes glycolysis and malignant progression of CCA by activating the HK2/ERK signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  6. LAMC2 Drives Airway Remodeling in COPD via EMT Regulation Through the AKT Pathway.International journal of chronic obstructive pulmonary disease · 2026
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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

9 authors at 7 institutions in 4 countries.

Anuradha KirtoniaAmity Institute of Molecular Medicine and Stem Cell Research (AIMMSCR), Amity University Uttar Pradesh, Sector-125, Noida, 201313, India.
Amit Kumar PandeyAmity Institute of Biotechnology, Amity University Haryana, Manesar, Haryana, 122413, India.
Balaji RamachandranDepartment of Molecular Oncology, Cancer Institute (WIA), Chennai, Tamil Nadu, India.
Durga Prasad MishraCell Death Research Laboratory, Endocrinology Division, CSIR-Central Drug Research Institute, Lucknow, Uttar Pradesh, 226031, India.
David W DawsonDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, 90095, USA.
Gautam SethiDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, 117600, Singapore.
Trivadi S GanesanLaboratory for Cancer Biology, Department of Medical Oncology, Sri Ramachandra Institute of Higher Education and Research, Chennai, 610016, India.
H Phillip KoefflerCancer Science Institute (CSI) of Singapore, National University of Singapore, Singapore, 117600, Singapore.
Manoj GargAmity Institute of Molecular Medicine and Stem Cell Research (AIMMSCR), Amity University Uttar Pradesh, Sector-125, Noida, 201313, India. mgarg@amity.edu.ORCID http://orcid.org/0000-0002-3492-2957
Amity University · INCancer Institute (WIA) · INCedars-Sinai Medical Center · USCentral Drug Research Institute · INNational University of Singapore · SGSri Ramachandra Institute of Higher Education and Research · INUniversity of California, Los Angeles · US

Funding

Indian Council of Medical Research No.3/2/2/59/2020-NCD-IIIScience and Engineering Research Board ECR/2016/001519
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is correlated with poor outcomes because of limited therapeutic options. Laminin-5 gamma-2 (LAMC2) plays a critical role in key biological processes. However, the detailed molecular mechanism and potential roles of LAMC2 in PDAC stay unexplored. The present study examines the essential role and molecular mechanisms of LAMC2 in the tumorigenesis of PDAC. Here, we identified that LAMC2 is significantly upregulated in microarray cohorts and TCGA RNA sequencing data of PDAC patients compared to non-cancerous/normal tissues. Patients with higher transcript levels of LAMC2 were correlated with clinical stages; dismal overall, as well as, disease-free survival. Additionally, we confirmed significant upregulation of LAMC2 in a panel of PDAC cell lines and PDAC tumor specimens in contrast to normal pancreatic tissues and cells. Inhibition of LAMC2 significantly decreased cell growth, clonogenic ability, migration and invasion of PDAC cells, and tumor growth in the PDAC xenograft model. Mechanistically, silencing of LAMC2 suppressed expression of ZEB1, SNAIL, N-cadherin (CDH2), vimentin (VIM), and induced E-cadherin (CDH1) expression leading to a reversal of mesenchymal to an epithelial phenotype. Interestingly, co-immunoprecipitation experiments demonstrated LAMC2 interaction with epidermal growth factor receptor (EGFR). Further, stable knockdown of LAMC2 inhibited phosphorylation of EGFR, ERK1/2, AKT, mTOR, and P70S6 kinase signaling cascade in PDAC cells. Altogether, our findings suggest that silencing of LAMC2 inhibited PDAC tumorigenesis and metastasis through repression of epithelial-mesenchymal transition and modulation of EGFR/ERK1/2/AKT/mTOR axis and could be a potential diagnostic, prognostic, and therapeutic target for PDAC.

Indexed as

Carcinoma, Pancreatic DuctalLamininMAP Kinase Signaling SystemPancreatic NeoplasmsProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCarcinogenesisCell Adhesion MoleculesCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionErbB ReceptorsHumansCell Adhesion MoleculesEGFR protein, humanErbB ReceptorsLAMC2 protein, humanLamininMTOR protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAKTEGFREpithelial-mesenchymal transitionLAMC2MigrationmTORPancreatic carcinomaXenograft model

Identifiers

PMID35699794
PMCPMC11073089
OpenAlexW4282826354

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.