Evidence map›Paper›PMID 37575080›Full record

ArticleCancer biology & therapy2023

SIRT1 promotes the progression and chemoresistance of colorectal cancer through the p53/miR-101/KPNA3 axis.

Xiao-Wei Wang, Ying-Hao Jiang, Wei Ye, Chun-Fa Shao, Jian-Jin Xie, Xia Li

Open access · goldAbstract read
In one paragraph

Article in Cancer biology & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 3% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. The role of KPNA3 in multiple myeloma: implications for targeting nuclear import.Apoptosis : an international journal on programmed cell death · 2026
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  6. The role of NADFrontiers in oncology · 2026
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  11. The role of SIRT1 in the development of gastrointestinal tumors.Frontiers in cell and developmental biology · 2025
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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 1 institution in 1 country.

Xiao-Wei WangDepartment of Anorectal Surgery, The First People's Hospital of Wenling, Wenling, China.
Ying-Hao JiangDepartment of Anorectal Surgery, The First People's Hospital of Wenling, Wenling, China.
Wei YeDepartment of Anorectal Surgery, The First People's Hospital of Wenling, Wenling, China.
Chun-Fa ShaoDepartment of Anorectal Surgery, The First People's Hospital of Wenling, Wenling, China.
Jian-Jin XieDepartment of Anorectal Surgery, The First People's Hospital of Wenling, Wenling, China.
Xia LiDepartment of Anorectal Surgery, The First People's Hospital of Wenling, Wenling, China.ORCID 0000-0002-5868-8907
The First People's Hospital of Wenling · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionSirtuin 1 (SIRT1) is a key modulator in several types of cancer, including colorectal cancer (CRC). Here, we probed into the molecular mechanism of SIRT1 regulating the development and chemoresistance of CRC.

methodsDifferentially expressed genes related to the growth, metastasis and chemoresistance of CRC were identified by bioinformatics analysis. The expression of SIRT1 in clinical tissues from CRC patients and CRC cell lines was detected by RT-qPCR. Interactions among SIRT1, p53, miR-101 and KPNA3 were analyzed. The effect of SIRT1 on the cell viability, migration, invasion, epithelial-mesenchymal transformation and chemoresistance to 5-FU was evaluated using loss-function investigations in CRC cells. Finally, a xenograft model of CRC and a metastasis model were constructed for further exploration of the roles of SIRT1 in vivo.

resultsSIRT1 was elevated in CRC tissues and cell lines. SIRT1 decreased p53 via deacetylation, and consequently downregulated the expression of miR-101 while increasing that of the miR-101 target gene KPNA3. By this mechanism, SIRT1 enhanced the proliferation, migration, invasion, epithelial-mesenchymal transformation, and resistance to 5-FU of CRC cells. In addition, in vivo data also showed that SIRT1 promoted the growth, metastasis and chemoresistance to 5-FU of CRC cells via regulation of the p53/miR-101/KPNA3 axis.

conclusionsIn conclusion, SIRT1 can function as an oncogene in CRC by accelerating the growth, metastasis and chemoresistance to 5-FU of CRC cells through the p53/miR-101/KPNA3 axis.

Indexed as

Colorectal NeoplasmsMicroRNAsalpha KaryopherinsCell Line, TumorCell ProliferationDrug Resistance, NeoplasmFluorouracilGene Expression Regulation, NeoplasticHumansSirtuin 1Tumor Suppressor Protein p53alpha KaryopherinsFluorouracilKPNA3 protein, humanMicroRNAsMIRN101 microRNA, humanSIRT1 protein, humanSirtuin 1Tumor Suppressor Protein p53chemoresistancecolorectal cancerepithelial-mesenchymal transformationKPNA3metastasisMiR-101p53SIRT1

Identifiers

PMID37575080
PMCPMC10431729
OpenAlexW4385798811

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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.