Evidence map›Paper›PMID 37697257›Full record

ArticleBMC cancer2023

Increased TCP11 gene expression can inhibit the proliferation, migration and promote apoptosis of cervical cancer cells.

Fang Wang, Shuyan Song, Bingxuan Guo, Yangyang Li, Huijuan Wang, Shaowei Fu, Luyue Wang, Xiangyi Zhe, Hongtao Li, Dongmei Li and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

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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

12 authors at 3 institutions in 2 countries.

Fang Wang *Department of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, Xinjiang, 832002, China.
Shuyan Song *Department of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, Xinjiang, 832002, China.
Bingxuan Guo *Department of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, Xinjiang, 832002, China.
Yangyang LiDepartment of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, Xinjiang, 832002, China.
Huijuan WangDepartment of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, Xinjiang, 832002, China.
Shaowei FuDepartment of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, Xinjiang, 832002, China.
Luyue WangDepartment of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, Xinjiang, 832002, China.
Xiangyi ZheDepartment of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, Xinjiang, 832002, China. 342480821@qq.com.
Hongtao LiDepartment of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, Xinjiang, 832002, China.
Dongmei LiDepartment of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, Xinjiang, 832002, China.
Renfu ShaoCentre for Bioinnovation, School of Science, Technology and Engineering, University of the Sunshine Coast, Maroochydore, 4556, Australia.
Zemin PanDepartment of Biochemistry and Molecular Biology, School of Medicine, Xinjiang Endemic and Ethnic Disease and Education Ministry Key Laboratory, Shihezi University, Shihezi, Xinjiang, 832002, China. panteacher89@sina.com.
Shihezi University · CNBeijing Chest Hospital · CNUniversity of the Sunshine Coast · AU

Funding

International Science and Technology Collaboration Projector of Xinjiang Production and Construction Corps 2019BC007the National Natural Science Foundation of China 82060518
6 · The paper itself

Abstract

backgroundCervical cancer is a common gynecological malignancy. Gene microarray found that TCP11 gene was highly expressed in cervical cancer. However, the effect of TCP11 gene on the proliferation, apoptosis and migration of cervical cancer cells and its underlying molecular mechanisms are unclear.

methodsGEPIA database, tissue microarray, western blot and qRT-PCR were used to analyze the expression of TCP11 gene in cervical cancer tissues and cells and its relationship with patients' survival rate. The cell cycle and apoptosis were detected by flow cytometry, and the expressions of cell cycle and apoptosis related molecules and EMT-related molecules were detected by Western blot and qRT-PCR.

resultsThe results showed that TCP11 gene was highly expressed in cervical cancer tissues and cells compared with normal cervical tissues and cells, and its expression was positively correlated with patients' survival rate. The results of proliferation and migration assays showed that TCP11 overexpression inhibited the proliferation and migration of HeLa and SiHa cells. The results showed that TCP11 overexpression blocked the cell cycle of HeLa and SiHa cells, decreased the expression of CDK1 and Cyclin B1, and increased the apoptosis and the expression of caspase-3, cleaved-caspase-3 and cleaved-PARP. TCP11 overexpression increased the protein and mRNA expression of EMT-related molecules ZO-1 and E-cadherin. Conversely, TCP11 knockdown promoted the proliferation of HeLa and SiHa cells and the migration of HeLa cells.

conclusionsTCP11 overexpression significantly inhibited the occurrence and development of cervical cancer cells, it may be a potentially beneficial biomarker for cervical cancer.

Indexed as

Membrane ProteinsUterine Cervical NeoplasmsApoptosisCaspase 3Cell DivisionFemaleGene ExpressionHeLa CellsHumansCaspase 3Membrane ProteinsTCP11 protein, humanApoptosisCell cycleCervical cancerMigration and proliferationTCP11 gene

Identifiers

PMID37697257
PMCPMC10496356
OpenAlexW4386609330

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.