In mechanical experiments, SNHG16 upregulated HK2, the target gene of miR-490-3p, by competitively sponging miR-490-3p and then promoted endometrial carcinoma proliferation and glycolysis.
Results presented that SNHG16 expression was increased in the ECa tissue and cells, and the ectopic SNHG16 overexpression was closely correlated with the poor survival rate and recurrence free survival of ECa.
Hypermutated/ultramutated cancers constitute the majority of UDC/DDC, suggesting a crucial difference with other high-risk histologies of endometrial carcinoma.
Loss of MDC1 expression (defined as negative nuclear staining) was found in 8.9% (38/426) of ECs and was significantly associated with the loss of MRE11 homolog, double-strand break repair nuclease, RAD50 double-strand break repair protein and nibrin complex components.
Loss of MDC1 expression (defined as negative nuclear staining) was found in 8.9% (38/426) of ECs and was significantly associated with the loss of MRE11 homolog, double-strand break repair nuclease, RAD50 double-strand break repair protein and nibrin complex components.
Loss of MDC1 expression (defined as negative nuclear staining) was found in 8.9% (38/426) of ECs and was significantly associated with the loss of MRE11 homolog, double-strand break repair nuclease, RAD50 double-strand break repair protein and nibrin complex components.
Due to deficient homologous recombination DNA repair, MDC1-negative ECs might show an increased sensitivity to poly(ADP-ribose) polymerase-inhibitory therapy.
Preoperative use of metformin in obese women with endometrioid endometrial cancer (EEC) reduces tumor proliferation and inhibits the mammalian target of rapamycin pathway, though is only effective in select cases.
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.
In conclusion, the hub genes and pathways identified in the present study contributed to the understanding of carcinogenesis and progression of EC at the mechanistic and molecular-biological level.
In this study, we investigated the anti-tumor effect of inhibitors of these pathways in vitro by assessing the effect of the combination of ATM or ATR inhibitors and conventional DNA-damaging therapy (doxorubicin (DXR), cisplatin (CDDP), and irradiation) on endometrial cancer cells.
In this study, we investigated the anti-tumor effect of inhibitors of these pathways in vitro by assessing the effect of the combination of ATM or ATR inhibitors and conventional DNA-damaging therapy (doxorubicin (DXR), cisplatin (CDDP), and irradiation) on endometrial cancer cells.
To assess the effect of skincare product use on the risk of pre- and postmenopausal breast cancer, estrogen receptor positive (ER+) and negative (ER-) breast cancer and cancer of the endometrium.
In the present study, abnormal p53 accumulation was analyzed using immunohistochemical techniques in endometrial carcinoma samples derived from 221 consecutive patients.
Extracted tampon DNA underwent the following: 1) low-coverage whole genome sequencing (LC-WGS) to assess copy number, 2) pyrosequencing to measure percent promotor methylation of HOXA9, RASSF1, and CDH13 and 3) next generation sequencing (NGS) to identify mutations in 19 genes associated with EC identified through The Cancer Genome Atlas.
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.
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.
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.