LINC00626 promotes the malignant process of colorectal cancer metastasis through the JAK1/STAT3/ KHSRP axis.

Objective To examine the regulation of malignant progression of colorectal cancer by LINC00626 via the JAK1/STAT3/KHSRP signaling axis and its molecular mechanism. Methods 96 individuals diagnosed with colorectal cancer at our hospital during June 11, 2021 and June 11, 2023 were chosen as research subjects, and their cancerous tissue and nearby normal tissue were collected. Cultivate colorectal cancer cell lines (SW620, HCT116, HT29, DLD-1, LOVO, Caco-2) and normal colorectal cells (NCM460) in vitro, and detect the expression of LINC00626 and KHSRP in colorectal cancer tissue and cell lines using qRT-PCR. Screening out cell lines infected with lentivirus, SW620 and HCT116 cell lines were transfected with knockdown lentivirus and its control, while HT29 and DLD-1 cell lines were transfected with overexpressing lentivirus and its control, respectively. Select stable transfected cell lines for cell function experiments to detect proliferation, migration, and invasion abilities. Detection of the effect of LINC00626 on the growth and migration of colorectal cancer tumors in live mouse experiments. The expression level of KHSRP protein in stable labeled cells was determined using a western blot analysis. Rescue experimental research on the regulatory relationship between LINC00626 and KHSRP. Results qRT-PCR showed low expression of LINC00626 and high expression of KHSRP in colorectal cancer tissues and cell lines. Cell function experiments showed that compared with the sh-NC group, the sh-LINC00626 group promoted cell proliferation, migration, and invasion in SW620 and HCT116 cells, while the overexpression group showed the opposite. Cell rescue experiments showed that, LINC00626+KHSRP significantly reversed the promotion effects of knocking down LINC00626 on cell proliferation, migration, and invasion. In the nude mouse experiment, compared with the sh-NC group, the sh-LINC00626 group showed a significant increase in tumor volume and weight, cell proliferation rate, and the number of lung metastases from colorectal cancer in the nude mice, Overexpression results in the opposite. The signal pathway experiment revealed that relative to the sh-NC group, the expression levels of JAK1 and STAT3 mRNA in the sh-LINC00626 group were significantly increased, whereas the results in the overexpression group were the opposite. Conclusion LINC00626 suppression the malignant progression of colorectal cancer metastasis through the JAK1/STAT3/KHSRP signaling axis. [ABSTRACT FROM AUTHOR]