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Biomedical Science
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Research/Clinical
Abstract
Colorectal carcinoma (CRC) is the second leading cause of cancer-related mortality in the United States. While localized CRC has a 90% five-year survival rate, this drops sharply to 14% upon metastasis. Metastasis occurs in approximately 40–50% of CRC cases and requires cancer cells to acquire anoikis resistance—a critical adaptation allowing survival after detachment from the extracellular matrix, enabling migration and colonization of secondary sites. Understanding the molecular mechanisms driving anoikis resistance, particularly those linked to altered glucose metabolism, is essential for developing targeted therapies for metastatic CRC.
Cancer cells frequently exhibit the Warburg Effect, a metabolic adaptation favoring glycolysis over oxidative phosphorylation even in the presence of oxygen. This shift supports tumor cell proliferation and may enhance survival under anchorage-independent conditions. Our preliminary findings suggest that the long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1), which is overexpressed in CRC and associated with poor prognosis, plays a central role in glucose metabolism and metastasis.
To investigate UCA1’s function, we utilized isogenic CRC cell lines derived from primary (SW480) and metastatic (SW620) tumors. Stable UCA1-overexpressing (SW480+UCA1) and UCA1-knockdown (SW620+shUCA1) models were developed. Phenotypic assays demonstrated that UCA1 overexpression enhances invasion, migration, proliferation, and colony formation, while its knockdown reduces these traits. Additionally, UCA1 overexpression was linked to increased glucose uptake, lactate production, and anchorage-independent survival, indicating its role in metabolic reprogramming to promote anoikis resistance.
Furthermore, studies evaluate UCA1’s impact under anchorage-independent conditions by assessing changes in cell cycle progression, pro-survival signaling, and stemness markers. Glucose metabolism will also be analyzed using Seahorse XFp metabolic profiling. These findings may uncover UCA1 as a critical regulator of CRC metastasis and a potential therapeutic target.
Recommended Citation
Bracho, Ricardo Pequeno; Shaham, Salique Hassan; Abuchard Anaya, Yamile; Leslie, Sophia; Doxtater, Kyle; Chauhan, Subhash; Hafeez, Bilal; Oraby, Tamer; and Tripathi, Manish K., "UCA1 as a Key Regulator of the Warburg Effect during Anoikis Resistance in Colorectal Cancer Metastasis" (2025). Research Symposium. 134.
https://scholarworks.utrgv.edu/somrs/2025/posters/134
Included in
Biochemical Phenomena, Metabolism, and Nutrition Commons, Cancer Biology Commons, Cell Biology Commons, Medical Cell Biology Commons, Medical Molecular Biology Commons, Molecular Biology Commons
UCA1 as a Key Regulator of the Warburg Effect during Anoikis Resistance in Colorectal Cancer Metastasis
Colorectal carcinoma (CRC) is the second leading cause of cancer-related mortality in the United States. While localized CRC has a 90% five-year survival rate, this drops sharply to 14% upon metastasis. Metastasis occurs in approximately 40–50% of CRC cases and requires cancer cells to acquire anoikis resistance—a critical adaptation allowing survival after detachment from the extracellular matrix, enabling migration and colonization of secondary sites. Understanding the molecular mechanisms driving anoikis resistance, particularly those linked to altered glucose metabolism, is essential for developing targeted therapies for metastatic CRC.
Cancer cells frequently exhibit the Warburg Effect, a metabolic adaptation favoring glycolysis over oxidative phosphorylation even in the presence of oxygen. This shift supports tumor cell proliferation and may enhance survival under anchorage-independent conditions. Our preliminary findings suggest that the long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1), which is overexpressed in CRC and associated with poor prognosis, plays a central role in glucose metabolism and metastasis.
To investigate UCA1’s function, we utilized isogenic CRC cell lines derived from primary (SW480) and metastatic (SW620) tumors. Stable UCA1-overexpressing (SW480+UCA1) and UCA1-knockdown (SW620+shUCA1) models were developed. Phenotypic assays demonstrated that UCA1 overexpression enhances invasion, migration, proliferation, and colony formation, while its knockdown reduces these traits. Additionally, UCA1 overexpression was linked to increased glucose uptake, lactate production, and anchorage-independent survival, indicating its role in metabolic reprogramming to promote anoikis resistance.
Furthermore, studies evaluate UCA1’s impact under anchorage-independent conditions by assessing changes in cell cycle progression, pro-survival signaling, and stemness markers. Glucose metabolism will also be analyzed using Seahorse XFp metabolic profiling. These findings may uncover UCA1 as a critical regulator of CRC metastasis and a potential therapeutic target.
