Evidence map›Paper›PMID 41614410›Full record

ArticleOncology reports2026

TRIM46 deficiency‑induced DNA damage enhances the sensitivity of cisplatin in non‑small cell lung cancer by regulating the Akt signaling pathway.

Song Jin, Dandan Zhang, Zhicheng Liao, Lingpei Yu, Yuanyuan Wang, Pengcheng Jia, Minmin Pan, Yifan Li, Jizhou Zhang

Abstract read
In one paragraph

Article in Oncology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

9 authors.

Song Jin *Department of Oncology, Wenzhou Traditional Chinese Medicine Hospital of Zhejiang Chinese Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Dandan Zhang *Traditional Chinese Medicine Research and Experimental Center, Wenzhou Traditional Chinese Medicine Hospital of Zhejiang Chinese Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Zhicheng LiaoDepartment of Oncology, Wenzhou Traditional Chinese Medicine Hospital of Zhejiang Chinese Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Lingpei YuDepartment of Encephalopathy, Rui'an Traditional Chinese Medicine Hospital, Wenzhou, Zhejiang 325000, P.R. China.
Yuanyuan WangDepartment of Gastroenterology, Yueqing Traditional Chinese Medicine Hospital, Yueqing, Zhejiang 325600, P.R. China.
Pengcheng JiaDepartment of Oncology, Wenzhou Traditional Chinese Medicine Hospital of Zhejiang Chinese Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Minmin PanDepartment of Oncology, Wenzhou Traditional Chinese Medicine Hospital of Zhejiang Chinese Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Yifan LiDepartment of Oncology, Wenzhou Traditional Chinese Medicine Hospital of Zhejiang Chinese Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Jizhou ZhangDepartment of Oncology, Wenzhou Traditional Chinese Medicine Hospital of Zhejiang Chinese Medical University, Wenzhou, Zhejiang 325000, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is one of the most aggressive malignancies worldwide. Non‑small cell lung cancer (NSCLC), in particular, is characterized by a poor 5‑year survival rate, which is largely attributable to cisplatin (DDP) resistance. However, the molecular mechanisms underlying DDP resistance are still not fully understood. Tripartite motif 46 (TRIM46) is implicated in promoting the progression of lung adenocarcinoma and enhancing chemoresistance. Nevertheless, its specific role in DDP resistance remains elusive. The present study aimed to investigate the role of TRIM46 in DDP resistance. Immunohistochemistry and TUNEL staining were employed to detect the expression of TRIM46 and apoptotic cells in tumor tissues. Lentiviruses were used to construct TRIM46 overexpression and knockdown vectors in A549 and A549/DDP cells. Cell proliferation, apoptosis and DNA damage were measured by Cell Counting Kit‑8, flow cytometry and comet assay, respectively. Subcutaneous implantation model through injection of A549/DDP cells with TRIM46 knockdown was performed in BALB/c nude female mice, followed by DDP treatment. The results revealed that TRIM46 was highly expressed in DDP‑resistant NSCLC tumor tissues and positively associated with DDP resistance. TRIM46 overexpression attenuated the DDP‑induced apoptosis and DNA damage of A549 cells. Meanwhile, the knockdown of TRIM46 enhanced the DDP‑induced apoptosis and DNA damage in A549/DDP cells. Mechanistically, TRIM46 activated the Akt signaling, thus inhibiting the expression of caspase 3 and cleaved‑caspase 3 as well as increasing the expression level of DNA repair protein RAD51. Furthermore, TRIM46 deficiency inhibited tumor growth and increased DDP sensitivity

Indexed as

Carcinoma, Non-Small-Cell LungCisplatinDrug Resistance, NeoplasmLung NeoplasmsA549 CellsAnimalsApoptosisCell Line, TumorCell ProliferationDNA DamageFemaleGene Expression Regulation, NeoplasticHumansMiceMice, Inbred BALB CMice, NudeCisplatinProto-Oncogene Proteins c-aktapoptosischemoresistancecisplatinDNA damagetripartite motif 46

Identifiers

PMID41614410
PMCPMC12892016

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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.