Evidence map›Paper›PMID 40926062›Full record

ArticleBritish journal of cancer2025

SLC7A11-AS1 contributes to prolonged activation of activin A/Smad signaling by suppressing PPM1A myristoylation in pancreatic cancer.

Mengmeng Li, Zhicheng Zhang, Qingzhu Yang, Fei Wang, Xuemei Huang, Huan Nie, Kai Li, Huanjie Yang

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In one paragraph

Article in British journal of cancer, 2025. 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

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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

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3 · Its place in the literature

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No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Mengmeng LiSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.ORCID http://orcid.org/0009-0005-0386-6955
Zhicheng ZhangHarbin Medical University, Harbin, China.
Qingzhu YangCollege of Life Science and Agriculture Forestry, Qiqihar University, Qiqihar, China.
Fei WangSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Xuemei HuangSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Huan NieSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Kai LiSchool of Medicine and Health, Harbin Institute of Technology, Harbin, China. likai2017@hit.edu.cn.
Huanjie YangSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China. yanghj@hit.edu.cn.ORCID http://orcid.org/0000-0001-8320-2182

Funding

National Natural Science Foundation of China (National Science Foundation of China) 52372267National Natural Science Foundation of China (National Science Foundation of China) 82172582
6 · The paper itself

Abstract

backgroundActivin A/Smad signaling plays an important role in promoting cancer stemness and chemoresistance in pancreatic ductal adenocarcinoma (PDAC), however the precise regulation on the termination of this pathway has not been fully understood.

methodsLncRNA SLC7A11-AS1 interacting proteins were identified through RNA pull-down followed by LC-MS/MS. The protein interaction was analyzed by co-immunoprecipitation. The expressions of SLC7A11-AS1 and activin A in tissue microarray were analyzed by FISH and immunofluerescence. Tumor xenograft mice models were established for in vivo experiments.

resultsOverexpression of SLC7A11-AS1 enhanced the activin A-induced Smad2/3 phosphorylation and promoted cancer stemness properties in PDAC cells. Mechanically, SLC7A11-AS1 interacts with scaffold protein RSL1D1. This interaction disrupts PPM1A myristoylation by suppressing the recruitment of PPM1A and myristoyltransferase NMT1 to RSL1D1, leading to prolonged activation of activin A/Smad signaling through the delay of Smad2/3 dephosphorylation. Co-overexpression of SLC7A11-AS1 and activin A were found in pancreatic patients, and related with the extremely short survival periods. Knockdown of SLC7A11-AS1 and blockade of activin A signaling significantly reduced gemcitabine resistance in PDAC in vitro and in vivo.

conclusionsSLC7A11-AS1 contributes to prolonged activation of activin A/Smad signaling by suppressing PPM1A myristoylation. Targeting both SLC7A11-AS1 and activin A may offer a potential therapeutic strategy for overcoming gemcitabine resistance in PDAC.

Indexed as

ActivinsCarcinoma, Pancreatic DuctalPancreatic NeoplasmsProtein Phosphatase 2CRNA, Long NoncodingSmad ProteinsAnimalsCell Line, TumorDeoxycytidineDrug Resistance, NeoplasmFemaleGemcitabineGene Expression Regulation, NeoplasticHumansMaleMiceactivin AActivinsDeoxycytidineGemcitabinePPM1A protein, humanProtein Phosphatase 2CRNA, Long NoncodingSmad Proteins

Identifiers

PMID40926062
PMCPMC12603235

What Socratic holds

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Registered trials

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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 Socratic graph.