ArticleOncology research2025
TIMM8A-TIMM13 Complex Exerts Oncogenic Functions in Lung Cancer.
Article in Oncology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
Who cites it
1 citing paper in PubMed.
- Loss of TIMM8A Inhibits Breast Cancer Progression Through Promoting HSPA9 Ubiquitination and Degradation via Competitive Interaction with RNF4.International journal of molecular sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Lung cancer represents a major global healthcare challenge, characterized by high annual incidence and mortality rates worldwide. Although targeted therapies for lung cancer have advanced, treatment outcomes for advanced-stage patients remain suboptimal. This investigation examines the role of the translocase of the inner mitochondrial membrane (TIMM)8A-TIMM13 complex in lung cancer and evaluates its potential as a novel therapeutic target. Methods: A co-immunoprecipitation (Co-IP) assay was conducted to verify the interaction between TIMM8A and TIMM13. Differential gene expression analysis of TIMM8A or TIMM13 was executed using the TNMplot database, with survival estimates derived from the Kaplan-Meier plotter. Lung cancer cell proliferation was evaluated through Cell Counting Kit 8 (CCK-8) and colony formation assays, while cell migration was assessed via Transwell assay. RNA sequencing identified the downstream effectors of TIMM13. RNAi technology facilitated the inhibition of TIMM8A or TIMM13 expression, which was measured through immunoblotting or qRT-PCR. Results: This investigation revealed that components of the TIMM8A-TIMM13 complex exhibited elevated expression in human lung cancer tissues, correlating with disease progression and poor overall survival rates among lung cancer patients. The suppression of either TIMM8A or TIMM13 inhibited cell proliferation and migration. Mechanistic studies through transcriptome analysis identified cell cycle-related pathways as potential key downstream effectors of the TIMM8A-TIMM13 complex. Subsequent experiments confirmed that the TIMM8A-TIMM13 complex significantly regulated the expression of cyclin D1 (CCND1) and cyclin-dependent kinase 6 (CDK6) complex. Conclusion: The elevated expression of TIMM8A-TIMM13 complex components plays a crucial role in lung cancer cell growth, suggesting its potential as a promising therapeutic target for lung cancer treatment.
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Registered trials
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 Socratic graph.