For mechanism investigation, hsa_circ_0001038 could sponge miR-337-3p to release its suppression on cyclin-M3 (CNNM3) and metastasis-associated in colon cancer 1 (MACC1), thereby promoting CC cell growth and invasive potential, respectively.
This review aims to summarize and discuss the immunological role of HLA-E in the context of HPV infection and immune system evasion, and the oncogenic process of cervical cancer.
The overexpression of miR‑411 and low expression of STK17A were correlated with high efficacy of radiotherapy. miR‑411 and STK17A had predictive value for the efficacy of radiotherapy; miR‑411 was the protective factor and STK17A was a risk factor for prognosis of cervical cancer.
Next, we demonstrated that over-expression of miR-214 or knockdown of MKK3 can inhibit the growth, proliferation, invasion and migration of cervical cancer in vitro and in vivo.
Furthermore, the leucine-rich repeat containing the eight family member E (LRRC8E) could bind with miR-625-5p, and its expression was negatively modulated by miR-625-5p, whereas positively regulated by LINC00958 in CC.
Our findings provide a better understanding of the molecular mechanism underlying circAMOTL1 in cervical cancer and indicated circAMOTL1/miR-485-5p/AMOTL1 as a promising novel therapeutic strategy for the treatment of this disease.
In the cervical cancer cell (HeLa) with endogenous high TRIM3 expression, increased expression of miR-454-3p obviously inhibited TRIM3 expression and then manipulating cell growth and apoptosis, down-regulating the expression of P53 and cleaved caspase-3 via P38 MAPK signaling.
Taken together, the results of this study showed that TIPE1 serves as an oncogene by restricting p53 activity in the development of cervical cancer, suggesting that TIPE1 will provide a new potential target for cervical cancer therapy and can be used as a biomarker to predict patient prognosis.
The expression of p53was negative in normal cervix, while there were 48 p53-positive cases (61.54%) and 30 p53-negative cases (38.46%) in patients with cervical cancer (p<0.05).
In this report, we aimed to explore the roles of gene polymorphisms affecting x-ray repair cross complementing 1 (XRCC1), the tumor protein p53 (TP53), and fibroblast growth factor receptor 3 (FGFR3) in the context of susceptibility to cervical cancer.
CP-31398, a styrylquinazoline, emerges from a screen for therapeutic agents that restore the wild-type DNA-binding conformation of mutant p53 to suppress tumors in vivo, but its effects on cervical cancer (CC) remain unknown.
Furthermore, we found that transcription factor TP53 could promote the expression of miR-3647-5p, suggesting that the dysfunction of miR-3647-5p in cervical cancer may be related to TP53.
In this report, we aimed to explore the roles of gene polymorphisms affecting x-ray repair cross complementing 1 (XRCC1), the tumor protein p53 (TP53), and fibroblast growth factor receptor 3 (FGFR3) in the context of susceptibility to cervical cancer.
Inactivating mutations of the tumor suppressor gene Liver Kinase B1 (<i>LKB1</i>) are frequently detected in non-small-cell lung cancer (NSCLC) and cervical carcinoma.