Manon Chadourne, Crystal Griffith, Neel Jasani, Xiaonan Xu, Emily Brennan, Olga Vera, Nicol Mecozzi, Kaizhen Wang, Alex M Jaeger, Florian A Karreth
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CDH3-AS1 antisense RNA enhances P-cadherin translation and acts as a tumor suppressor in melanoma.
Thousands of regulatory non-coding RNAs (ncRNAs) have been annotated, yet their roles in gene regulation and cancer progression remain unclear. Mapping the landscape of ncRNA expression during melanoma progression revealed that ncRNAs represented nearly half of the deregulated genes, with antisense RNAs (asRNAs) comprising a large portion. CDH3-AS1, the most downregulated asRNA, overlaps the CDH3 gene, which encodes P-cadherin, a key cell adhesion protein that is reduced in melanoma. Overexpression of CDH3-AS1 increased cell aggregation and reduced xenograft tumor growth, mimicking the effects of CDH3. CDH3-AS1 interacted with CDH3 mRNA, increased ribosome occupancy, and enhanced P-cadherin translation through a mechanism resembling SINEB2 sequence to up-regulate translation (SINEUP)-mediated translational control. asRNAs complementary to 5' UTRs generally increase the ribosome occupancy of their cognate mRNAs, suggesting broader translational control through this mechanism. This study revealed CDH3-AS1-mediated enhancement of P-cadherin translation as a tumor-suppressive axis in melanoma and highlighted the broader potential of asRNAs as regulators of protein translation.
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Cell Reports publishes high-quality research across the life sciences and focuses on new biological insight as its primary criterion for publication. The journal offers three primary article types: Reports, which are shorter single-point articles, research articles, which are longer and provide deeper mechanistic insights, and resources, which highlight significant technical advances or major informational datasets that contribute to biological advances. Reviews covering recent literature in emerging and active fields are also accepted.
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