Abstract:
OBJECTIVE To explore the expression of long non-coding RNA (LncRNA) TTTY15/MIF-AS1 in cervical cancer (CC) tissues and its relationship with autophagy in human papilloma virus (HPV) infection.
METHODS A total of 82 patients with CC admitted to Obstetrics and Gynecology Department of Tianjin Fifth Central Hospital were enrolled as CC group between Dec. 2018 and Dec. 2021, while 50 patients with low-grade squamous intraepithelial lesions (LSIL) and 50 patients with high-grade squamous intraepithelial lesions (HSIL) who underwent cervical examinations during the same period were enrolled as LSIL group and HSIL group, respectively. The relative expression levels of LncRNA TTTY15 and LncRNA MIF-AS1 in cervical tissues were detected by immunohistochemistry. The autophagy pathway genesautophagy-related gene-12 (ATG12), BECN1, microtubule-associated protein 1 light chain 3 beta (MAP1LC3B) were amplified by real-time quantitative polymerase chain reaction (RT-PCR), and their relative expression levels were calculated by 2
-ΔΔct method.
RESULTS There were significant differences in relative expression levels of LncRNA TTTY15, LncRNA MIF-AS1, ATG12, BECN1 and MAP1LC3B among CC group, HSIL group and LSIL group (
P<0.05), which were the highest in CC group, followed by HSIL group and LSIL group (
P<0.05). There were significant differences relative expression level of LncRNA TTTY15 among CC patients with different lymph node metastasis, tumor size and differentiation status (
P<0.05). There were significant differences relative expression level of LncRNA MIF-AS1 in CC patients with different lymph node metastasis and differentiation status (
P<0.05). The relative expression levels of LncRNA TTTY15 and LncRNA MIF-AS1 in cervical tissues were positively correlated with relative expressions of autophagy pathway genes (ATG12, BECN1, MAP1LC3B) (
P<0.05).
CONCLUSION LncRNA TTTY15 and LncRNA MIF-AS1 are involved in the pathological progression of cervical cancer in high-risk HPV infection, and the mechanism may be related to autophagy pathway.