Evidence map›Paper›PMID 35655161›Full record

ArticleBMC cancer2022

MUC3A promotes the progression of colorectal cancer through the PI3K/Akt/mTOR pathway.

Wei Su, Baijie Feng, Lina Hu, Xianzhi Guo, Minghua Yu

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  13. Exploring the Key Signaling Pathways and ncRNAs in Colorectal Cancer.International journal of molecular sciences · 2024
    Review
  14. Article
  15. The essential roles of lncRNAs/PI3K/AKT axis in gastrointestinal tumors.Frontiers in cell and developmental biology · 2024
    Review
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  18. Review
  19. Article
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

5 authors at 2 institutions in 1 country.

Wei Su *Department of Oncology, Fudan University Pudong Medical Center, Shanghai Pudong Hospital, 2800 Gongwei Road, Shanghai, 201399, China.
Baijie Feng *Department of Oncology, Fudan University Pudong Medical Center, Shanghai Pudong Hospital, 2800 Gongwei Road, Shanghai, 201399, China.
Lina HuDepartment of Oncology, Fudan University Pudong Medical Center, Shanghai Pudong Hospital, 2800 Gongwei Road, Shanghai, 201399, China.
Xianzhi GuoDepartment of Oncology, Fudan University Pudong Medical Center, Shanghai Pudong Hospital, 2800 Gongwei Road, Shanghai, 201399, China.
Minghua YuDepartment of Oncology, Fudan University Pudong Medical Center, Shanghai Pudong Hospital, 2800 Gongwei Road, Shanghai, 201399, China. minghua_md@fudan.edu.cn.
Pudong Medical Center · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mucin 3A (MUC3A) is overexpressed in colorectal cancer (CRC) and associated with poor prognosis, but the related mechanism remains unclear. Our study found that MUC3A promotes the progression of CRC by activating the PI3K/Akt/mTOR signaling pathway. Knockout of MUC3A significantly inhibited the proliferation of CRC cells and induced G1 phase arrest by upregulating p21 protein, an important cell cycle regulator. Moreover, knockout of MUC3A significantly inhibited invasion ability and enhanced the sensitivity to the chemotherapeutic agent 5-FU. Furthermore, we found that knockout of MUC3A repressed the PI3K/Akt/mTOR pathway through RNA-seq. Treatment with the PI3K/Akt/mTOR pathway inhibitor rapamycin successfully eliminated the difference in proliferation, invasion and chemoresistance between MUC3A knockout cells and control cells. Our study suggests that MUC3A is a potential oncogene that promotes the proliferation, invasion, and chemotherapy resistance of CRC. Moreover, CRC patients with high expression of MUC3A may benefit from rapamycin treatment.

Indexed as

Colorectal NeoplasmsPhosphatidylinositol 3-KinasesCell MovementCell ProliferationHumansMucin-3Proto-Oncogene Proteins c-aktSirolimusTOR Serine-Threonine KinasesMTOR protein, humanMUC3A protein, humanMucin-3Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSirolimusTOR Serine-Threonine KinasesAktCancer progressionCell cycleColorectal cancermTOR pathwayMUC3API3K

Identifiers

PMID35655161
PMCPMC9161576
OpenAlexW4281983889

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.