CAMOR and specific oncogene-driven lncRNAs mediate carcinogenic functions downstream of MYC, mutant KRAS, and mutant TP53
- 1Mossakowski Medical Research Institute PAS, Warsaw, Poland
Abstract
Purpose Long non-coding RNAs (lncRNAs) are important regulators of tumor biology, but their dependence on major oncogenic drivers and cancer specificity remain poorly characterized. We aimed to identify lncRNAs regulated by MYC, mutant KRAS, and mutant TP53 across colorectal, lung, and pancreatic cancer and to determine their functional relevance and molecular mechanism. Methods We performed an integrative analysis of lncRNA expression profiles driven by MYC, mutant KRAS, and mutant TP53 across colorectal, lung, and pancreatic cancer cell lines. Candidate lncRNAs were functionally characterized using assays of cancer cell viability, migration, and clonogenicity. Expression in patient-derived tumor and normal tissues and downstream molecular pathways were investigated. Results MYC was associated with the most extensive lncRNA regulation, with expression patterns largely independent of tissue origin. MYC-dependent LINC00997 and the previously uncharacterized AC104447.1, as well as specifically KRAS-dependent RAKRAR (RASSF3 antisense KRAS regulated lncRNA) promoted cancer cell viability, migration, and clonogenicity. LINC00997 and AC104447.1 expression was elevated in specific tumor types compared to normal tissues. We identified CAMOR (CARNMT1 Antisense Multiple-Oncoprotein Regulated lncRNA), a pan-cancer lncRNA upregulated by all three oncogenic drivers. CAMOR promoted viability and migration specifically in cancer cells across analyzed cell lines and tumor types. Mechanistically, CAMOR and neighboring CARNMT1 form a negative feedback regulatory loop affecting CAMOR oncogenic activity. Distinct downstream gene expression signatures suggested that the studied lncRNAs act through different regulatory processes. Conclusion Our findings expand the repertoire of oncogenic lncRNAs and demonstrate that integrating multiple oncogenic contexts enables identification of both driver-specific and broadly acting lncRNAs, providing a framework for identifying lncRNAs that may contribute to cancer development and represent potential diagnostic or therapeutic targets.
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BibTeX
@misc{grzes2026camor,
title = {{CAMOR and specific oncogene-driven lncRNAs mediate carcinogenic functions downstream of MYC, mutant KRAS, and mutant TP53}},
author = {M. Grzes and A. Jaiswar and W. Kazmierczak and T. Olesinski and M. Nowak-Niezgoda and D. Walerych},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.04.749381},
url = {https://www.biorxiv.org/content/10.64898/2026.09.04.749381v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - CAMOR and specific oncogene-driven lncRNAs mediate carcinogenic functions downstream of MYC, mutant KRAS, and mutant TP53
AU - M. Grzes
AU - A. Jaiswar
AU - W. Kazmierczak
AU - T. Olesinski
AU - M. Nowak-Niezgoda
AU - D. Walerych
PY - 2026
DA - 2026/09/04
PB - bioRxiv
DO - 10.64898/2026.09.04.749381
UR - https://www.biorxiv.org/content/10.64898/2026.09.04.749381v1
AB - Purpose Long non-coding RNAs (lncRNAs) are important regulators of tumor biology, but their dependence on major oncogenic drivers and cancer specificity remain poorly characterized. We aimed to identify lncRNAs regulated by MYC, mutant KRAS, and mutant TP53 across colorectal, lung, and pancreatic cancer and to determine their functional relevance and molecular mechanism. Methods We performed an integrative analysis of lncRNA expression profiles driven by MYC, mutant KRAS, and mutant TP53 across colorectal, lung, and pancreatic cancer cell lines. Candidate lncRNAs were functionally characterized using assays of cancer cell viability, migration, and clonogenicity. Expression in patient-derived tumor and normal tissues and downstream molecular pathways were investigated. Results MYC was associated with the most extensive lncRNA regulation, with expression patterns largely independent of tissue origin. MYC-dependent LINC00997 and the previously uncharacterized AC104447.1, as well as specifically KRAS-dependent RAKRAR (RASSF3 antisense KRAS regulated lncRNA) promoted cancer cell viability, migration, and clonogenicity. LINC00997 and AC104447.1 expression was elevated in specific tumor types compared to normal tissues. We identified CAMOR (CARNMT1 Antisense Multiple-Oncoprotein Regulated lncRNA), a pan-cancer lncRNA upregulated by all three oncogenic drivers. CAMOR promoted viability and migration specifically in cancer cells across analyzed cell lines and tumor types. Mechanistically, CAMOR and neighboring CARNMT1 form a negative feedback regulatory loop affecting CAMOR oncogenic activity. Distinct downstream gene expression signatures suggested that the studied lncRNAs act through different regulatory processes. Conclusion Our findings expand the repertoire of oncogenic lncRNAs and demonstrate that integrating multiple oncogenic contexts enables identification of both driver-specific and broadly acting lncRNAs, providing a framework for identifying lncRNAs that may contribute to cancer development and represent potential diagnostic or therapeutic targets.
ER -