Altered gene expression by C1orf106 in endometrial cancer cells.
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE298672 | GEO | 2025/06/21
REPOSITORIES: GEO
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Project description:Chromosome 1 open reading frame 106 (C1orf106) has been shown to be elevated in lung adenocarcinoma. However, its expression and function in papillary thyroid cancer (PTC) are totally unknown. To explore the role of C1orf106 in PTC, we analyzed the gene expression in TPC1 cells with or without C1orf106 overexpression.
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Project description:<p>Endometrial diseases are common gynecological diseases that disorder women of childbearing age and perimenopausal women, including endometrial polyps (EP), endometrial cancer (EC), and endometrial hyperplasia (EH). Clinically, biopsy or imaging methods are usually used to screen and diagnose endometrial diseases, but due to their invasiveness and heterogeneity, a noninvasive, convenient, objective and accurate biomarker is needed for the differential diagnosis of EP and EC or EH. In the present study, serum samples from 396 patients with endometrial disease and 225 healthy volunteers were analyzed by UPLC-Q-TOF/MS non-targeted lipidomics. A combination of multivariate (Orthogonal partial least-squares discriminant analysis) and univariate (Student t-test) analyses were used to identify and qualify 6, 8, and 7 potential biomarkers in serum from patients with EP, EC, and EH, respectively. With the aid of logistic regression algorithm and receiver operating characteristic (ROC) curve analysis, A biomarker panel including four specific EP biomarkers, 6-Keto-PGF1α, PA(37:4), LysoPC(20:1) and PS (36:0), had good classification and diagnostic ability in distinguishing EP from EC or EH. The biomarker panel can be used as a rapid diagnostic method to assist imaging examination to effectively differentially diagnose endometrial diseases, and provide a reference for clinicians in the identification and diagnosis of endometrial diseases. </p>
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Project description:Endometrial cancer is the most commonly diagnosed gynecologic malignancy in women after breast, lung and colorectal cancer. Despite numerous scientific advances, the incidence and mortality rate of endometrial cancer is on the rise. Considerable research effort has therefore been placed on understanding the pathogenesis of this disease to combat this growing issue. There is now emerging evidence to suggest a putative role for dysregulation of the renin angiotensin system (RAS) and in particular the (pro)renin receptor ((P)RR), in the ontogenesis of endometrial cancer. Support for this notion arises from previous literature implicating (P)RR in cancer pathophysiology (e.g., breast cancer and pancreatic carcinoma) by virtue of its role in proliferation, angiogenesis, fibrosis, migration and invasion. In view of these data, we aimed to investigate the functional role of (P)RR in human endometrial cancer progression and development. To this end, we employed an siRNA-mediated knock down approach to abrogate (P)RR expression in the immortalized endometrial epithelial cell lines; Ishikawa, AN3CA and HEC-1A to explore the role of (P)RR in cellular proliferation and cellular viability. To further extend these analyses we also carried out a sophisticated proteomic screen, that investigated the potential pathways via which (P)RR is acting in endometrial cancer physiology. These data confirmed that (P)RR is critical for endometrial cell cancer development, contributing to both its proliferative capacity and in the maintenance cell viability. This is likely mediated through proteins such as MGA, SLC4A7, SLC7A11 or DHRS2, which were reduced following (P)RR knockdown. These putative protein interactions/pathways, which rely on the presence of (P)RR, are likely to contribute to endometrial cancer progression and could therefore, represent several novel therapeutic targets in the treatment of this cancer. Finally we contend that (P)RR, in its soluble form (s(P)RR) in blood, may have substantial potential as a novel biomarker for cancer diagnosis and prognosis prediction going forward.
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Project description:A specific form of endometrial cancer (EC) can develop in breast cancer patients previously treated with tamoxifen (ET), an antagonist of estrogen receptor (ER) α that inhibits proliferation of ER positive breast cancer. ET tumors have a different phenotype than endometrial tumors which typically develop de novo without previous exposure to tamoxifen (EN). Here we aimed to identify specific protein markers that could serve as specific molecular targets in either phenotype. A set of total 45 formalin-fixed paraffin-embedded (FFPE) endometrial tumor tissue and adjacent myometrial tissue samples were analyzed using LC-MS/MS in SWATH-MS mode. We found that calcyphosin (CAPS) levels were elevated in EN tumors compared to ET tumors. The higher CAPS level in EC tissue invading to myometrium support its relationship to EC aggressiveness. Further, stathmin (STMN1) levels were found significantly elevated in ET vs. EN tumors and significantly associated with patient survival. This finding connects elevated levels of this cell cycle regulating, proliferation-associated protein with tamoxifen exposure. In a summary, using SWATH-MS we show that CAPS and STMN1 should be recognized as clinicopathologically different EC markers of which STMN1 is specifically connected with a previous tamoxifen exposition.
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Project description:To investigate the function NCAPG in the regulation in endometrial cancer, we established HEC-1-A cell lines in which NCAPG has been knocked down by RNAi.
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