Evidence map›Paper›PMID 35614441›Full record

ArticleCancer cell international2022

PGM1 suppresses colorectal cancer cell migration and invasion by regulating the PI3K/AKT pathway.

Zhewen Zheng, Xue Zhang, Jian Bai, Long Long, Di Liu, Yunfeng Zhou

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

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  7. Functional identification ofFrontiers in veterinary science · 2023
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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 3 institutions in 1 country.

Zhewen Zheng *Department of Radiation Oncology and Medical Oncology, Zhongnan Hospital of Wuhan University, 169 Donghu Road, Wuchang District, Wuhan, Hubei, People's Republic of China.
Xue Zhang *Department of General Practice, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, People's Republic of China.
Jian BaiDepartment of Anesthesiology, Peking University Third Hospital, Beijing, 100191, People's Republic of China.
Long LongDepartment of Radiation Oncology and Medical Oncology, Zhongnan Hospital of Wuhan University, 169 Donghu Road, Wuchang District, Wuhan, Hubei, People's Republic of China.
Di LiuDepartment of Radiation Oncology and Medical Oncology, Zhongnan Hospital of Wuhan University, 169 Donghu Road, Wuchang District, Wuhan, Hubei, People's Republic of China.
Yunfeng ZhouDepartment of Radiation Oncology and Medical Oncology, Zhongnan Hospital of Wuhan University, 169 Donghu Road, Wuchang District, Wuhan, Hubei, People's Republic of China. yfzhouwhu@163.com.ORCID http://orcid.org/0000-0003-4328-6646
Wuhan University · CNCapital Medical University · CNPeking University · CN

Funding

National Natural Science Foundation of China 81472799National Natural Science Foundation of China No. 82103553Research Foundation of Beijing Friendship Hospital No.yyqdkt2020-6
6 · The paper itself

Abstract

backgroundPhosphoglucomutase 1 (PGM1) is known for its involvement in cancer pathogenesis. However, its biological role in colorectal cancer (CRC) has remained unknown. Here, we studied the functions and mechanisms of PGM1 in CRC.

methodsWe verified PGM-1 as a differentially expressed gene (DEG) by employing a comprehensive strategy of TCGA-COAD dataset mining and computational biology. Relative levels of PGM-1 in CRC tumors and adjoining peritumoral tissues were determined by qRT-PCR, western blotting (WB), and immunohistochemical (IHC) staining in a tissue microarray. PGM1 functions were analyzed by CCK8, EdU, colony formation, cell cycle, apoptosis, and Transwell migration and invasion assays. The influence of PGM1 was further investigated by studying tumor formation in vivo.

resultsThe levels of PGM1 mRNA and protein were both reduced in CRC tissues, and the reductions were related to CRC pathology and overall survival. PGM1 knockdown stimulated both cell proliferation and colony formation, and inhibited cell cycle arrest and apoptosis, while overexpression of PGM1 produced the opposite effects in CRC cells both in vivo and in vitro. Furthermore, the effects of PGM1 were related to the PI3K/ AKT pathway.

conclusionWe verified that PGM1 suppresses CRC progression via the PI3K/AKT pathway. These results suggest the potential for targeting PGM1 in treatment of CRC.

Indexed as

ApoptosisColorectal cancerPhosphoglucomutase 1PrognosisProliferation

Identifiers

PMID35614441
PMCPMC9134613
OpenAlexW4281480146

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.