Evidence map›Paper›PMID 38824479›Full record

ArticleApoptosis : an international journal on programmed cell death2024

TBC1D10B promotes tumor progression in colon cancer via PAK4‑mediated promotion of the PI3K/AKT/mTOR pathway.

Xiao-Jv Chi, Yi-Bei Song, Haoran Zhang, Li-Qiang Wei, Yong Gao, Xue-Jing Miao, Shu-Ting Yang, Chun-Yu Lin, Dong Lan, Xiquan Zhang

Abstract read
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In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2024. 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
–field-weighted citation impact
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.

  1. Article
  2. Article
  3. The Role of the p21-Activated Kinase Family in Tumor Immunity.International journal of molecular sciences · 2025
    Review
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

10 authors.

Xiao-Jv Chi *Department of Clinical Laboratory, First Affiliated Hospital of Guangxi Medical University, Key Laboratory of Clinical Laboratory Medicine of Guangxi Department of Education, Guangxi Zhuang Autonomous Region, 6 Shuangyong Road, Nanning, 530021, China.
Yi-Bei Song *Department of Clinical Laboratory, First Affiliated Hospital of Guangxi Medical University, Key Laboratory of Clinical Laboratory Medicine of Guangxi Department of Education, Guangxi Zhuang Autonomous Region, 6 Shuangyong Road, Nanning, 530021, China.
Haoran Zhang *Department of Gastrointestinal Surgery, First Affiliated Hospital of Jinan University, 613 Huangpu Avenue West, Guangzhou, 510632, China.
Li-Qiang WeiDepartment of Clinical Laboratory, First Affiliated Hospital of Guangxi Medical University, Key Laboratory of Clinical Laboratory Medicine of Guangxi Department of Education, Guangxi Zhuang Autonomous Region, 6 Shuangyong Road, Nanning, 530021, China.
Yong GaoDepartment of Clinical Laboratory, First Affiliated Hospital of Guangxi Medical University, Key Laboratory of Clinical Laboratory Medicine of Guangxi Department of Education, Guangxi Zhuang Autonomous Region, 6 Shuangyong Road, Nanning, 530021, China.
Xue-Jing MiaoDepartment of Clinical Laboratory, First Affiliated Hospital of Guangxi Medical University, Key Laboratory of Clinical Laboratory Medicine of Guangxi Department of Education, Guangxi Zhuang Autonomous Region, 6 Shuangyong Road, Nanning, 530021, China.
Shu-Ting YangDepartment of Clinical Laboratory, First Affiliated Hospital of Guangxi Medical University, Key Laboratory of Clinical Laboratory Medicine of Guangxi Department of Education, Guangxi Zhuang Autonomous Region, 6 Shuangyong Road, Nanning, 530021, China.
Chun-Yu LinDepartment of Clinical Laboratory, First Affiliated Hospital of Guangxi Medical University, Key Laboratory of Clinical Laboratory Medicine of Guangxi Department of Education, Guangxi Zhuang Autonomous Region, 6 Shuangyong Road, Nanning, 530021, China.
Dong LanDepartment of Medical Oncology, First Affiliated Hospital of Guangxi Medical University, Guangxi Zhuang Autonomous Region, 6 Shuangyong Road, Nanning, 530021, China. landong@stu.gxmu.edu.cn.
Xiquan ZhangDepartment of Oncology, Jiangxi provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, 330006, China. Zhangxiquan1243@126.com.

Funding

Guangxi Health Department Research Project z20190853the First Affiliated Hospital of Guangxi Medical University Clinical Research Climbing Program YYZS2020023the Project for the Promotion of Young and Middle-aged University Teachers' Basic Research Ability in Guangxi 2020KY03016
6 · The paper itself

Abstract

This study aimed to explore the expression, function, and mechanisms of TBC1D10B in colon cancer, as well as its potential applications in the diagnosis and treatment of the disease.The expression levels of TBC1D10B in colon cancer were assessed by analyzing the TCGA and CCLE databases. Immunohistochemistry analysis was conducted using tumor and adjacent non-tumor tissues from 68 colon cancer patients. Lentiviral infection techniques were employed to silence and overexpress TBC1D10B in colon cancer cells. The effects on cell proliferation, migration, and invasion were evaluated using CCK-8, EDU, wound healing, and Transwell invasion assays. Additionally, GSEA enrichment analysis was used to explore the association of TBC1D10B with biological pathways related to colon cancer. TBC1D10B was significantly upregulated in colon cancer and closely associated with patient prognosis. Silencing of TBC1D10B notably inhibited proliferation, migration, and invasion of colon cancer cells and promoted apoptosis. Conversely, overexpression of TBC1D10B enhanced these cellular functions. GSEA analysis revealed that TBC1D10B is enriched in the AKT/PI3K/mTOR signaling pathway and highly correlated with PAK4. The high expression of TBC1D10B in colon cancer is associated with poor prognosis. It influences cancer progression by regulating the proliferation, migration, and invasion capabilities of colon cancer cells, potentially acting through the AKT/PI3K/mTOR signaling pathway. These findings provide new targets and therapeutic strategies for the treatment of colon cancer.

Indexed as

ApoptosisCell MovementCell ProliferationColonic NeoplasmsGTPase-Activating Proteinsp21-Activated KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesAdaptor Proteins, Signal TransducingCell Line, TumorDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansAdaptor Proteins, Signal TransducingGTPase-Activating ProteinsMTOR protein, humanp21-Activated KinasesPAK4 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTBC1D10B protein, humanTOR Serine-Threonine KinasesColon cancerPI3K-Akt signalingTBC1D10B

Identifiers

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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.