Evidence map›Paper›PMID 33045679›Full record

ArticleTranslational oncology2021

Overlapping targets exist between the Par-4 and miR-200c axis which regulate EMT and proliferation of pancreatic cancer cells.

Archana Katoch, Vijay Lakshmi Jamwal, Mir Mohd Faheem, Sriram Kumar, Shantibhusan Senapati, Govind Yadav, Sumit G Gandhi, Anindya Goswami

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Translational oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Archana KatochAcademy of Scientific & Innovative Research (AcSIR), New Delhi, India; Cancer Pharmacology Division, Indian Institute of Integrative Medicine (CSIR), Canal Road, Jammu, Jammu and Kashmir 180001, India.
Vijay Lakshmi JamwalAcademy of Scientific & Innovative Research (AcSIR), New Delhi, India; Plant Biotechnology and System Biology Division, CSIR-Indian Institute of Integrative Medicine, Jammu 180001, India.
Mir Mohd FaheemCancer Pharmacology Division, Indian Institute of Integrative Medicine (CSIR), Canal Road, Jammu, Jammu and Kashmir 180001, India.
Sriram KumarDepartment of Biotechnology, Rajalakshmi Engineering College (Anna University), Rajalakshmi Nagar, Thandalam, Chennai 602105, Tamil Nadu, India.
Shantibhusan SenapatiTumor Microenvironment and Animal Models Lab, Institute of Life Sciences (ILS), Nalco Square Bhubaneswar, Orissa 751023, India.
Govind YadavCentral Laboratory Animal Facility (Animal House), CSIR-Indian Institute of Integrative Medicine, Jammu 180001, India.
Sumit G GandhiAcademy of Scientific & Innovative Research (AcSIR), New Delhi, India; Plant Biotechnology and System Biology Division, CSIR-Indian Institute of Integrative Medicine, Jammu 180001, India. Electronic address: sumit@iiim.ac.in.
Anindya GoswamiAcademy of Scientific & Innovative Research (AcSIR), New Delhi, India; Cancer Pharmacology Division, Indian Institute of Integrative Medicine (CSIR), Canal Road, Jammu, Jammu and Kashmir 180001, India. Electronic address: agoswami@iiim.ac.in.
Indian Institute of Integrative Medicine · INAcademy of Scientific and Innovative Research · INAnna University, Chennai · INInstitute of Life Sciences · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The last decade has witnessed a substantial expansion in the field of microRNA (miRNA) biology, providing crucial insights into the role of miRNAs in disease pathology, predominantly in cancer progression and its metastatic spread. The discovery of tumor-suppressing miRNAs represents a potential approach for developing novel therapeutics. In this context, through miRNA microarray analysis, we examined the consequences of Prostate apoptosis response-4 (Par-4), a well-established tumor-suppressor, stimulation on expression of different miRNAs in Panc-1 cells. The results strikingly indicated elevated miR-200c levels in these cells upon Par-4 overexpression. Intriguingly, the Reverse Phase Protein Array (RPPA) analysis revealed differentially expressed proteins (DEPs), which overlap between miR200c- and Par-4-transfected cells, highlighting the cross-talks between these pathways. Notably, Phospho-p44/42 MAPK; Bim; Bcl-xL; Rb Phospho-Ser807, Ser811; Akt Phospho-Ser473; Smad1/5 Phospho-Ser463/Ser465 and Zyxin scored the most significant DEPs among the two data sets. Furthermore, the GFP-Par-4-transfected cells depicted an impeded expression of critical mesenchymal markers viz. TGF-β1, TGF-β2, ZEB-1, and Twist-1, concomitant with augmented miR-200c and E-cadherin levels. Strikingly, while Par-4 overexpression halted ZEB-1 at the transcriptional level; contrarily, silencing of endogenous Par-4 by siRNA robustly augmented the Epithelial-mesenchymal transition (EMT) markers, along with declining miR-200c levels. The pharmacological Par-4-inducer, NGD16, triggered Par-4 expression which corresponded with increased miR-200c resulting in the ZEB-1 downregulation. Noteworthily, tumor samples obtained from the syngenic mouse pancreatic cancer model revealed elevated miR-200c levels in the NGD16-treated mice that positively correlated with the Par-4 and E-cadherin levels in vivo; while a negative correlation was evident with ZEB-1 and Vimentin.

Indexed as

EMTmiR-200cPar-4RPPA

Identifiers

PMID33045679
PMCPMC7557890
OpenAlexW3091913308

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.