Summary. It has been reported that HITT can inhibit colon cancer. However, the role of HITT in gastric cancer (GC) is unknown. Our preliminary sequencing data revealed the altered expression of HITT in GC and its close correlation with miR-602, suggesting the involvement of HITT and its potential interaction with miR-602 in GC. This study explored the role of HITT and its crosstalk with miR-602 in GC. In this study, the expression of HITT, premature and mature miR-602 in paired GC and normal tissues (62 patients) was detected by RT-qPCR. RNA pull-down assay was performed to evaluate the direct interaction between HITT and mature miR-602. The subcellular location of HITT was assessed by nuclear fractionation assay. The role of HITT in regulating miR-602 maturation was explored by overexpression assay. Cell apoptosis was analyzed by flow cytometry. Our data illustrated that HITT was highly upregulated and mature miR-602 was downregulated in GC. No alteration in premature miR-602 in GC was observed. HITT was located in both nucleus and cytoplasm, and it can directly interact with miR-602. In addition, overexpression of HITT in GC cells increased the expression levels of mature miR-602 but not premature miR-602. Overexpression of HITT further increased GC cell apoptosis and suppressed the role of miR-602 in inhibiting GC cell apoptosis. In conclusion, HITT may promote GC cell apoptosis by suppressing the maturation of miR-602. Histol Histopathol 37, 1143-1150 (2022)

Key words: HITT, Gastric cancer, miR-602, Apoptosis

DOI: 10.14670/HH-18-495

©The Author(s) 2022. Open Access. This article is licensed under a Creative Commons CC-BY International License.