Evidence map›Paper›PMID 41085556›Full record

ArticleMolecular cancer research : MCR2026

Loss of Regulator of G Protein Signaling 11 Promotes Protumorigenic Features in Pancreatic Cancer.

Tejinder Kaur, Debasis Nayak, Arnav Joshi, Junan Li, Amy Hite, Rajgopal Govindarajan

Abstract read
In one paragraph

Article in Molecular cancer research : MCR, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Tejinder KaurDivision of Pharmaceutics and Pharmacology, College of Pharmacy, The Ohio State University, Columbus, Ohio.ORCID 0000-0002-5200-7461
Debasis NayakDivision of Pharmaceutics and Pharmacology, College of Pharmacy, The Ohio State University, Columbus, Ohio.ORCID 0000-0002-0602-4367
Arnav JoshiDivision of Pharmaceutics and Pharmacology, College of Pharmacy, The Ohio State University, Columbus, Ohio.ORCID 0000-0002-2719-2247
Junan LiDivision of Pharmaceutics and Pharmacology, College of Pharmacy, The Ohio State University, Columbus, Ohio.ORCID 0000-0003-0381-9356
Amy HiteBiomedical Informatics, The Ohio State University, Columbus, Ohio.ORCID 0000-0001-5503-7300
Rajgopal GovindarajanDivision of Pharmaceutics and Pharmacology, College of Pharmacy, The Ohio State University, Columbus, Ohio.ORCID 0000-0002-2958-5773

Funding

Anti-HIV NRTIs and the lysosomal toxicityR01GM143217 · NIGMS · OHIO STATE UNIVERSITY · PI GOVINDARAJAN, RAJGOPAL · 2021 to 2024
$1.3M
SLC29A3 lysosomal transporter in hematopoietic homeostasis and diseaseR01HL164443 · NHLBI · OHIO STATE UNIVERSITY · PI RAJGOPAL GOVINDARAJAN · 2024 to 2026
$1.2M
Evaluation of the antitumorigenic roles of miR-122 in pancreatic cancerR03CA262490 · NCI · OHIO STATE UNIVERSITY · PI GOVINDARAJAN, RAJGOPAL · 2022 to 2023
$158k
Division of Cancer Prevention, National Cancer Institute (DCP, NCI) R03CA262490National Heart, Lung, and Blood Institute (NHLBI) R01HL164443National Institute of General Medical Sciences (NIGMS) R01GM143217NCI NIH HHS R03 CA262490NHLBI NIH HHS R01 HL164443NIGMS NIH HHS R01 GM143217
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy associated with early metastasis, drug resistance, and poor outcomes. We previously demonstrated a putative tumor-suppressive role for concentrative nucleoside transporter 1 (CNT1) in PDAC. In this study, we demonstrate the regulator of G protein signaling (RGS) 11 as a key target of CNT1, with potent tumor-suppressive properties in PDAC. Compared with normal human pancreas, RGS11 expression is diminished in human PDAC tissues which correspond with the reduced patient survival times. In addition, quasimesenchymal pancreatic tumor cell lines with accelerated growth, metastatic propensity, and innate resistance to nucleoside analogs showed relatively lower RGS11 expression than their epithelial counterparts. Interestingly, RGS11 levels reversibly modulated the epithelial-mesenchymal transition of human PDAC cell lines influencing the chemotherapeutic sensitivities of anti-PDAC drugs. Additionally, stable lentiviral-mediated RGS11 expression reduced the cellular proliferation and colony establishment, increased the apoptotic index, and decreased the migratory and invasive abilities in quasimesenchymal tumor cell lines, whereas RGS11 depletion in epithelial tumor cell lines showed opposite effects. Global transcriptomic analysis revealed RGS11 replenishment in PDAC cells to suppress CD44-directed stemness features with significant reprogramming of the PDAC oncogenic landscape. Furthermore, RGS11 reduced the primary tumor burden and metastatic occurrence in a mouse model of PDAC. Together, these findings uncover RGS11 as a key target of CNT1 that exhibits therapeutic potential for intervention of aggressive PDAC. IMPLICATIONS: RGS11 identified as a downstream target of a gemcitabine transporter CNT1 exerts potent antitumorigenic features in PDAC with therapeutic and prognostic values.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsRGS ProteinsAnimalsCell Line, TumorCell ProliferationDeoxycytidineEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMembrane Transport ProteinsMicecif nucleoside transporterDeoxycytidineMembrane Transport ProteinsRGS Proteins

Identifiers

PMID41085556
PMCPMC12680025

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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.