Chen Yun, Ouyang Canhui, Liao Lingyun, Zhou Yun, Meng Fan, Liu Yao, Ye Jing
Department of Gastroenterology, The first Affiliated Hospital of Gannan Medical College, Ganzhou City, Jiangxi Province, PR China.
Office of Academic Affairs of Jiangxi University of Traditional Chinese Medicine, Nanchang City, Jiangxi Province, PR China.
Histol Histopathol. 2022 Nov;37(11):1143-1150. doi: 10.14670/HH-18-495. Epub 2022 Jul 19.
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.
据报道，高强度间歇训练（HITT）可抑制结肠癌。然而，HITT在胃癌（GC）中的作用尚不清楚。我们的初步测序数据显示，HITT在GC中的表达发生改变，且与miR-602密切相关，这表明HITT参与了GC的发生发展及其与miR-602的潜在相互作用。本研究探讨了HITT及其与miR-602的相互作用在GC中的作用。在本研究中，通过RT-qPCR检测了62例配对的GC组织和正常组织中HITT、前体miR-602和成熟miR-602的表达。进行RNA下拉实验以评估HITT与成熟miR-602之间的直接相互作用。通过细胞核分级分离实验评估HITT的亚细胞定位。通过过表达实验探讨HITT在调节miR-602成熟中的作用。通过流式细胞术分析细胞凋亡。我们的数据表明，GC中HITT高度上调，成熟miR-602下调。未观察到GC中前体miR-602的改变。HITT位于细胞核和细胞质中，并且它可以直接与miR-602相互作用。此外，在GC细胞中过表达HITT可增加成熟miR-602的表达水平，但不会增加前体miR-602的表达水平。过表达HITT进一步增加了GC细胞凋亡，并抑制了miR-602在抑制GC细胞凋亡中的作用。总之，HITT可能通过抑制miR-602的成熟来促进GC细胞凋亡。
