Furthermore, we validated that GHET1 down-regulation could inactivate AKT/mTOR and Wnt/β-catenin pathways, and that respective activation of these two pathways abrogated the inhibitive effect of GHET1 knockdown on CC cell growth, migration and EMT.
Furthermore, we also found that miR-4524b-5p could regulate the migration and invasion of cervical cancer by targeting WTX and that WTX could regulate the expression of β-catenin.
Mechanistic investigation showed PCAT6 activates Wnt/β-catenin signaling in CC cell lines by promoting the expression of β-catenin, cyclin D1 and c-myc.
Our work identifies MNK-eIF4E axis as a specific and critical regulator of β-catenin activity in cervical cancer but not normal cervical cells, and suggests that targeting MNK is a useful therapeutic strategy in cervical cancer.
The current study demonstrated that treatment with gefitinib decreased the protein expression levels of phosphorylated-GSK3β and β-catenin, which suggests that gefitinib may be a potential novel therapeutic strategy in CC by suppressing the Wnt/β-catenin signaling pathway and EMT to inhibit tumor metastasis in CC cells.
These findings provide evidence that the PI3K E542K and E545K/β-catenin/SIRT3 signaling axis regulates glucose metabolism and proliferation in cervical cancers with PIK3CA mutations, suggesting therapeutic targets in the treatment of cervical cancers.
Together, our data demonstrated that SOX17 restrained the proliferation and tumor formation by down-regulating the activity of the Wnt/β-catenin signaling pathway via trans-suppression of β-catenin in cervical cancer.
These results demonstrate that ICAT contributed to the progression of cervical cancer and may play a role in the regulation of EMT by distrupting the E-cadherin/β-catenin complex.
Our findings demonstrate that eIF4E/β-catenin signaling plays a positive regulatory role in the resistance of cervical cancer cell to chemotherapy and thus highlight the therapeutic value of eIF4E or β-catenin inhibition in overcoming chemoresistance.
This research unveiled the function of DEK in tumorigenesis and metastasis via the DEK/p-Ser9-GSK-3β/p-Tyr216-GSK-3β/β-catenin axis in cervical cancer and gave insights into DEK-targeting therapy for patients suffering from cervical cancer.
WNT2 overexpression in cervical cancer was associated with β-catenin activation and induction of EMT, which further contributed to metastasis in cervical cancer.
α-Actinin-4 induces the epithelial-to-mesenchymal transition and tumorigenesis via regulation of Snail expression and β-catenin stabilization in cervical cancer.
Taken together, our data demonstrate that EZH2 promotes cell proliferation and tumor formation in cervical cancer through activating the Wnt/β-catenin pathway by epigenetic silencing via GSK-3β and TP53.
Our study suggests that tigecycline is a useful addition to the treatment armamentarium for cervical cancer and targeting Wnt/β-catenin represents a potential therapeutic strategy in cervical cancer.
These data indicated that GSK3β may participated in HPV16 mediated deregulation of wnt/β-catenin and other signaling pathways promoting the progression and invasion of cervical cancers.