Evidence map›Paper›PMID 30915884›Full record

ArticleCancer biology & therapy2019

The role of lncRNA MSC-AS1/miR-29b-3p axis-mediated CDK14 modulation in pancreatic cancer proliferation and Gemcitabine-induced apoptosis.

Yunpeng Sun, Pengfei Wang, Wenjun Yang, Yunfeng Shan, Qiyu Zhang, Huanhuan Wu

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
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  12. Increased mAnnals of translational medicine · 2022
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  16. Role of hypermethylated-lncRNAs in the prognosis of bladder cancer patients.The Journal of international medical research · 2021
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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

6 authors at 2 institutions in 1 country.

Yunpeng Suna Department of Hepatobiliary Surgery , The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , China.
Pengfei Wangb Department of Gastrointestinal Surgery , The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , China.
Wenjun Yanga Department of Hepatobiliary Surgery , The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , China.
Yunfeng Shana Department of Hepatobiliary Surgery , The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , China.
Qiyu Zhanga Department of Hepatobiliary Surgery , The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , China.
Huanhuan Wuc Department of Post-anesthetic ICU , The First Affiliated Hospital of Wenzhou Medical University , Wenzhou , China.
First Affiliated Hospital of Wenzhou Medical University · CNWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) remains a leading cause of cancer-related death due to the failure of traditional therapies. In the present study, we attempted to construct a lncRNA-miRNA-mRNA network which may modulate PDAC cell proliferation and Gemcitabine-induced cell apoptosis starting from CDK14, a new member of the CDK family and an oncogene in many cancers. Based on TCGA data, a significant positive correlation was observed between lncRNA MSC-AS1 and CDK14. Moreover, MSC-AS1 expression was upregulated in PDAC tissues. Higher MSC-AS1 expression was correlated with poorer prognosis in patients with PDAC. MSC-AS1 knockdown in Panc-1 and BxPC-3 cells significantly inhibited the cell proliferation. Moreover, miR-29b-3p, which has been reported to act as a tumor suppressor, was predicted to bind to both MSC-AS1 and CDK14. Contrary to MSC-AS1, higher miR-29b-3p expression was correlated to better prognosis in patients with PDAC. In both PDAC cell lines, miR-29b-3p negatively regulated MSC-AS1 and CDK14. As confirmed using luciferase reporter gene and RIP assays, MSC-AS1 served as a ceRNA for miR-29b-3p to counteract miR-29b-mediated CDK14 repression. MSC-AS1 knockdown inhibited CDK14 protein levels and PDAC proliferation and enhanced gemcitabine-induced cell death and apoptosis while miR-29b-3p inhibition exerted an opposing effect; the effect of MSC-AS1 knockdown was partially attenuated by miR-29b-3p inhibition. Taken together, we demonstrated that MSC-AS1/miR-29b-3p axis modulates the cell proliferation and GEM-induced cell apoptosis in PDAC cell lines through CDK14. We provided a novel experimental basis for PDAC treatment from the perspective of lncRNA-miRNA-mRNA network.

Indexed as

Gene Expression Regulation, NeoplasticRNA, AntisenseRNA, Long NoncodingAdultAgedAntimetabolites, AntineoplasticApoptosisBasic Helix-Loop-Helix ProteinsCell Line, TumorCell MovementCell ProliferationCyclin-Dependent KinasesDeoxycytidineFemaleGemcitabineHumansAntimetabolites, AntineoplasticBasic Helix-Loop-Helix ProteinsCDK14 protein, humanCyclin-Dependent KinasesDeoxycytidineGemcitabineMicroRNAsMIRN29a microRNA, humanMSC protein, humanRNA, AntisenseRNA, Long NoncodingapoptosisCDK14lncRNA MSC-AS1miR-29b-3ppancreatic ductal adenocarcinoma (PDAC)proliferation

Identifiers

PMID30915884
PMCPMC6605982
OpenAlexW2924684777

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.