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Article Publish Status: FREE
Abstract Title:

Apigenin Targets MicroRNA-155, Enhances SHIP-1 Expression, and Augments Anti-Tumor Responses in Pancreatic Cancer.

Abstract Source:

Cancers (Basel). 2022 Jul 25 ;14(15). Epub 2022 Jul 25. PMID: 35892872

Abstract Author(s):

Kazim Husain, Krystal Villalobos-Ayala, Valentina Laverde, Oscar A Vazquez, Bradley Miller, Samra Kazim, George Blanck, Margaret L Hibbs, Gerald Krystal, Isra Elhussin, Joakin Mori, Clayton Yates, Tomar Ghansah

Article Affiliation:

Kazim Husain

Abstract:

Pancreatic cancer (PC) is a deadly disease with a grim prognosis. Pancreatic tumor derived factors (TDF) contribute to the induction of an immunosuppressive tumor microenvironment (TME) that impedes the effectiveness of immunotherapy. PC-induced microRNA-155 (miRNA-155) represses expression of Src homology 2 (SH2) domain-containing Inositol 5'-phosphatase-1 (SHIP-1), a regulator of myeloid cell development and function, thus impacting anti-tumor immunity. We recently reported that the bioflavonoid apigenin (API) increased SHIP-1 expression which correlated with the expansion of tumoricidal macrophages (TAM) and improved anti-tumor immune responses in the TME of mice with PC. We now show that API transcriptionally regulates SHIP-1 expression via the suppression of miRNA-155, impacting anti-tumor immune responses in the bone marrow (BM) and TME of mice with PC. We discovered that API reduced miRNA-155 in the PC milieu, which induced SHIP-1 expression. This promoted the restoration of myelopoiesis and increased anti-tumor immune responses in the TME of heterotopic, orthotopic and transgenic SHIP-1 knockout preclinical mouse models of PC. Our results suggest that manipulating SHIP-1 through miR-155 may assist in augmenting anti-tumor immune responses and aid in the therapeutic intervention of PC.

Study Type : In Vitro Study

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