We further identified that silencing of JPT1 abundance does not alter cellular response to metformin or basal cell proliferation, but that JPT1 abundance does decrease in response to metformin treatment in RL95-2 and ACI-181 EC cell lines.
VEGFA alternative splicing in endometrial cancer was regulated by RBM10, the expression of which was controlled by histone acetylation and DNA methylation.
The role of miR-27a-5p in EC migration and invasion was further investigated via transfection with miR-27a-5p mimics or inhibitor in Ishikawa and HEC-1A EC cell lines.
The aim of the study was to determine the changes in SEMA5A expression in endometrial cancer compared to normal endometrium and to indicate the potential use of SEMA5A as a molecular marker.
Notably, based on this network, it was found that LINC00261-hsa-mir-31 pair and LINC00261-hsa-mir-211 target pairs could be used as the potential prognostic markers of EC.
We also discuss the possible relationship between metformin and MK in the context of EC, the most common gynecological cancer worldwide, which incidence is rising rapidly, in parallel with the increase in obesity, T2DM and insulin resistance.
We think that it would be useful to determine the diagnosis, prediction of prognosis and identifying therapeutic targets of the highlighted proteins of our study that are K2C8, UAP56, GRP78 and CALR in endometrial cancer.
All in all, our research was the first endeavor to study the underlying mechanism of CHL1-AS1 in EC and confirmed that CHL1-AS1 regulated EC progression via targeting the miR-6076/CHL1 axis, offering new insight into treating EC.
The TERT promoter mutations were most frequently present in bladder cancer (68.6%), followed by central nervous system tumors (28.7%), thyroid cancer (15.4%), prostate cancer (9.3%), endometrial carcinoma (3.7%), rhabdomyosarcoma (1.4%), colorectal cancer (1%), epithelial ovarian carcinoma (0.7%) and breast cancer (0.7%).
Knockdown of ferrochelatase (FECH) in human endometrial cancer xenografts in nude mice was performed by transfection with FECH-siRNA mediated by PEI and ultrasound microbubbles alone or in combination; then, low-dose ALA was injected.
After adjusting for confounders, postmenopausal patients had higher total serum calcium (p=0.002) and albumin-corrected serum calcium (p=0.012) than premenopausal patients, endometrioid endometrial carcinoma (EEC) patients had higher total serum calcium than non-endometrioid endometrial carcinoma (NEEC) patients (p=0.037).
In addition, we identified 2 patients who had a deleterious germline mutation in Lynch syndrome genes (MLH1 and MLH2), and another 8 patients harbored germline mutations of 6 non-Lynch syndrome genes (MUTYH, GALNT12, POLE, MPL, ATM, and ERCC4) which may be associated with endometrial cancer.
The minor allele of rs1045242 in the TNFAIP8 gene was strongly associated with with EC risk (adjust OR: 1.636, 95% CI 1.107-2.417, P = 0.014). rs11064 SNPs correlated with TNFAIP8 protein expression in EC (P = 0.015).
There was no correlation between SERPINA3 protein in endometrial cancer cells and the age range at which women experienced menopause (<i>P</i> > 0.05).
Furthermore, we identified that CCL18 derived from TAMs upregulated KIF5B expression to promote EMT via activating the PI3K/AKT/mTOR signaling pathway in endometrial cancer.