ArticleCell death discovery2024
LncRNA MACC1-AS1 induces gemcitabine resistance in pancreatic cancer cells through suppressing ferroptosis.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The trial behind it
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Non-coding RNAs as master regulators of ferroptosis in cancer: mechanisms and clinical implications.Molecular cancer · 2026Review
- Ferroptosis: The dawn of reversing drug resistance in digestive cancers.Genes & diseases · 2026Review
- Development and validation of a gemcitabine sensitivity-related long noncoding RNA signature for predicting the prognosis and subtypes of bladder cancer.Translational andrology and urology · 2026Article
- Discovery of a Ferroptosis-Related lncRNA-miRNA-mRNA Gene Signature in Endometrial Cancer Through a Comprehensive Co-Expression Network Analysis.Current oncology (Toronto, Ont.) · 2026Article
- HSPB1/KDM1 A facilitates ANXA2 expression via hypomethylated DNA promoter to inhibit ferroptosis and enhance gemcitabine resistance in pancreatic cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Screening of PANoptosis regulator-associated long noncoding RNAs and construction of a survival prognostic model in cutaneous melanoma.Translational cancer research · 2025Article
- The Molecular Interplay Between p53-Mediated Ferroptosis and Non-Coding RNAs in Cancer.International journal of molecular sciences · 2025Review
- Solasodine suppresses nasopharyngeal carcinoma progression by inducing ferroptosis.Scientific reports · 2025Article
- Circulating non-coding RNAs as a tool for liquid biopsy in solid tumors.Epigenomics · 2025Review
- Prognostic risk stratification value of MACC1 expression in patients with gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Article
- MACC1 revisited - an in-depth review of a master of metastasis.Biomarker research · 2024Review
- Epigenetic modification of ferroptosis by non-coding RNAs in cancer drug resistance.Molecular cancer · 2024Review
- Mechanism of ferroptosis resistance in cancer cells.Cancer drug resistance (Alhambra, Calif.) · 2024Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDA) mortality is primarily attributed to metastasis and chemotherapy resistance. In this research, the long non-coding RNA MACC1-AS1 was studied, playing a significant role in regulating lipid oxidation processes. This regulation could further lead to the inhibition of ferroptosis induced by chemotherapeutic drugs, making it a contributing factor to gemcitabine resistance in PDA. In both gemcitabine-resistant PDA patients and mouse models, the elevated expression level of MACC1-AS1 in the tumors was noted. Additionally, overexpression of MACC1-AS1 in pancreatic cancer cells was found to enhance tolerance to gemcitabine and suppress ferroptosis. Proteomic analysis of drug-resistant pancreatic cells revealed that overexpressed MACC1-AS1 inhibited the ubiquitination degradation of residues in the protein kinase STK33 by MDM4. Furthermore, its accumulation in the cytoplasm activated STK33, further activating the ferroptosis-suppressing proteins GPX4, thereby counteracting gemcitabine-induced cellular oxidative damage. These findings suggested that the long non-coding RNA MACC1-AS1 could play a significant role in the ability of pancreatic cancer cells to evade iron-mediated ferroptosis induced by gemcitabine. This discovery holds promise for developing clinical therapeutic strategies to combat chemotherapy resistance in pancreatic cancer.
Identifiers
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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.