ArticleHuman cell2026
Hsa_circ_0003176: a key player in the m6A modification-mediated regulation of autophagy and glycolysis in cisplatin-resistant non-small cell lung cancer.
Article in Human cell, 2026. 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.
- Emerging functions of m6A-modified circRNAs and their targeting strategies in lung cancer.Frontiers in cell and developmental biology · 2026Review
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
Abstract
Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related mortality worldwide, with poor prognosis largely attributed to late-stage diagnosis and therapeutic resistance. Cisplatin (DDP) resistance is a major challenge in NSCLC treatment. Emerging evidence highlights the critical role of N6-methyladenosine (m6A) RNA modification in regulating cancer progression and drug resistance, with methyltransferase-like 3 (METTL3) serving as the key methyltransferase mediating m6A deposition on RNAs. In this study, we investigated the role of the circular RNA hsa_circ_0003176 in DDP-resistant NSCLC and its regulation by m6A modification. We found that hsa_circ_0003176 was significantly downregulated in DDP-resistant NSCLC cells and functioned as a tumor suppressor by promoting autophagy, inhibiting glycolysis, and reversing DDP resistance. Mechanistically, METTL3-mediated m6A modification suppressed hsa_circ_0003176 expression, while hsa_circ_0003176 directly targeted and destabilized ribosomal protein S6 kinase B1 (RPS6KB1) mRNA, a key regulator of mTORC1 signaling, thereby inhibiting NSCLC progression. In addition, in vivo xenograft models confirmed that hsa_circ_0003176 overexpression suppressed tumor growth and enhanced DDP sensitivity. Our study reveals the METTL3/m6A/hsa_circ_0003176/RPS6KB1 pathway as a critical pathway in NSCLC chemoresistance, offering novel therapeutic targets for overcoming DDP resistance.
Indexed as
Identifiers
41579303What Socratic holds
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.