Evidence map›Paper›PMID 38935235›Full record

ArticleHuman cell2024

KIN17 functions in DNA damage repair and chemosensitivity by modulating RAD51 in hepatocellular carcinoma.

Xueran Huang, Zichang Dai, Biyun Zeng, Xiangyan Xiao, Kashif Rafiq Zahid, Xiaocong Lin, Tiancai Liu, Tao Zeng

Abstract read
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In one paragraph

Article in Human cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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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

2 citing papers in PubMed.

  1. Article
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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

8 authors.

Xueran Huang *Department of Medical Laboratory, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524000, Guangdong, P. R. China.
Zichang Dai *Department of Clinical Laboratory, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, 310000, Zhejiang, China.
Biyun Zeng *School of Medical Technology, Guangdong Medical University, Dongguan, 523808, Guangdong, P. R. China.
Xiangyan XiaoDepartment of Medical Laboratory, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524000, Guangdong, P. R. China.
Kashif Rafiq ZahidDepartment of Radiation Oncology, Indiana University Melvin and Bren Simon Comprehensive Cancer Center, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Xiaocong LinInstitute of Biochemistry and Molecular Biology, Guangdong Medical University, Zhanjiang, 524023, Guangdong, P. R. China. congtoulin750325@126.com.
Tiancai LiuKey Laboratory of Antibody Engineering of Guangdong Higher Education Institutes, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, 510515, Guangdong, P. R. China. liutc@smu.edu.cn.
Tao ZengDepartment of Medical Laboratory, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524000, Guangdong, P. R. China. zengt@smu.edu.cn.ORCID http://orcid.org/0000-0001-8896-0361

Funding

Basic and Applied Basic Research Foundation of Guangdong Province 2023A1515010235Medical Science and Technology Foundation of Guangdong Province A2023168Medical Science and Technology Foundation of Guangdong Province B2021180National Natural Science Foundation of China 82372344Natural Science Foundation of Guangdong Province 2023A1515011925
6 · The paper itself

Abstract

The limited response of hepatocellular carcinoma (HCC) to chemotherapy drugs has always been a bottleneck in therapy. DNA damage repair is a major reason for chemoresistance. Previous studies have confirmed that KIN17 affects chemosensitivity. In this study, we examined the impact of KIN17 on chemotherapy response and DNA repair in HCC cells treated with oxaliplatin (L-OHP). We evaluated the expression and biological roles of KIN17 in HCC using bioinformatic analysis. The correlation between KIN17 and RAD51, particularly their nuclear expression levels, was evaluated using immunofluorescence, immunoblotting after nucleocytoplasmic separation in HCC cells, and immunohistochemistry of mouse xenograft tumors and human HCC tissues. The results indicated a significant increase in KIN17 expression in HCC tissues compared to normal tissues. The GSEA analysis revealed that upregulation of KIN17 was significantly associated with DNA damage repair. Knockdown of KIN17 led to increased DNA damage and reduced cellular survival after exposure to L-OHP. On the other hand, overexpression of KIN17 was linked to decreased DNA damage and improved cell survival following L-OHP treatment. Further experiments indicated that KIN17 affects the expression of RAD51, particularly in the nucleus. KIN17 plays a crucial role in influencing the sensitivity of HCC to chemotherapy by triggering the DNA repair response. Increased expression of KIN17 is associated with a poor prognosis for HCC patients, indicating that KIN17 could serve as a prognostic marker and therapeutic target for HCC.

Indexed as

Carcinoma, HepatocellularDNA DamageDNA RepairLiver NeoplasmsOxaliplatinRad51 RecombinaseAnimalsAntineoplastic AgentsCell Line, TumorDrug Resistance, NeoplasmGene ExpressionHumansMiceAntineoplastic AgentsOxaliplatinRAD51 protein, humanRad51 RecombinaseChemosensitivityDNA damage repairHepatocellular carcinomaKIN17RAD51

Identifiers

PMID38935235

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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.