sincalide and Ovarian-Neoplasms

Platinum is a commonly used drug for ovarian cancer (OvCa) treatment, but drug resistance limits its clinical application. This study intended to delineate the effects of adipocytes on platinum resistance in OvCa.. OvCa cells were maintained in the adipocyte-conditioned medium. Cell viability and apoptosis were detected by CCK-8 and flow cytometry, separately. Proliferation and apoptosis-related protein expression were assayed by western blot. The IC. Adipocytes promoted the viability and repressed cell apoptosis in OvCa, as well as enhancing platinum resistance, while the addition of IGF-1 R inhibitor reversed the effects of adipocytes on proliferation, apoptosis, and drug resistance of OvCa cells. Treatment with different concentrations of Ojeok-san (OJS) inhibited the adipocyte-induced platinum resistance in OvCa cells by suppressing IGF1. The combined treatment of OJS and cisplatin significantly inhibited tumour growth. In summary, OJS inhibited OvCa proliferation and platinum resistance by suppressing adipocyte paracrine IGF1 secretion.

Topics: Adipocytes; Animals; Cisplatin; Drug Resistance, Neoplasm; Female; Humans; Insulin-Like Growth Factor I; Mice; Ovarian Neoplasms; Sincalide

Ovarian cancer (OC) is a common clinical gynecological disease, which seriously threatens women's health and life. We investigated the roles of SPOCK2 in OC and its associated molecular mechanism in the current study.. The expressions and prognostic value of SPOCK2 in OC were identified using the clinical data and data from the GEPIA database. Then, SPOCK2 silence was implemented to search functions of SPOCK2 in OC cells. CCK-8 was used to examine cell proliferation. Cell apoptosis was detected by flow cytometry. The OC cell invasion and migration were evaluated by transwell assays.. Overexpressed SPOCK2 was identified in OC, which was correlated with poor prognosis and a shorter survival rate. SPOCK2 downregulation significantly suppressed OC cell proliferation, migration, and invasion, and cell apoptosis was markedly promoted by SPOCK2 silence. Meanwhile, SPOCK2 knockdown could effectively suppress Wnt/. SPOCK2 exerted crucial functions in OC progression and could serve as a promising candidate for OC targeted therapy.

Topics: beta Catenin; Carcinoma, Ovarian Epithelial; Cell Line, Tumor; Cell Movement; Cell Proliferation; Female; Gene Expression Regulation, Neoplastic; Humans; Ovarian Neoplasms; Proteoglycans; Sincalide; Wnt Signaling Pathway

Recent studies have revealed that long noncoding RNAs (lncRNAs) play a crucial role in tumor progression. Ovarian cancer is a common type of fatal gynecological cancer worldwide. This study aims to investigate how lncRNADSCAM-AS1 functions in the progression of ovarian cancer.. DSCAM-AS1 expression of both ovarian cancer cells and 56 paired of tissue samples was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Moreover, the function of DSCAM-AS1 was identified via transwell assay, wound healing assay, colony formation assay and proliferation assay in vitro. The underlying mechanism was explored through qRT-PCR and Western blot assay.. DSCAM-AS1 expression was remarkably upregulated in tumor tissues compared with that in the adjacent normal tissues. Besides, ovarian cancer proliferation, migration and invasion were promoted after overexpression of DSCAM-AS1 in vitro. Moreover, after overexpression of DSCAM-AS1, SOX4 was upregulated at mRNA and protein level in vitro. Furthermore, the expression of SOX4 in tumor tissues was positively correlated with the expression of DSCAM-AS1.. The above results suggested that DSCAM-AS1 can promote cell migration, invasion and proliferation in ovarian cancer by upregulating SOX4, which may offer a new therapeutic intervention for patients with ovarian cancer.

Topics: Cell Movement; Cell Proliferation; Disease Progression; Female; Humans; Neoplasm Invasiveness; Ovarian Neoplasms; Prognosis; RNA, Long Noncoding; RNA, Messenger; Sincalide; SOXC Transcription Factors; Up-Regulation

Cholecystokinin (CCK)-A and CCK-B/gastrin receptors were evaluated with in vitro receptor autoradiography in 406 human tumors of various origins using a sulfated 125I-labeled CCK decapeptide analogue 125I-(D-Tyr-Gly, Nle28,3l)-CCK 26-33 and 125I-labeled Leu15-gastrin as radioligands. CCK-B/gastrin receptors were found frequently in medullary thyroid carcinomas (92%), in small cell lung cancers (57%), in astrocytomas (65%), and in stromal ovarian cancers (100%). They were found occasionally in gastroenteropancreatic tumors, breast, endometrial, and ovarian adenocarcinomas. They were either not expressed or rarely expressed in colorectal cancers, differentiated thyroid cancers, non-small cell lung cancers, meningiomas, neuroblastomas, schwannomas, glioblastomas, lymphomas, renal cell cancers, prostate carcinomas, and the remaining neuroendocrine tumors (i.e., pituitary adenomas, pheochromocytomas, paragangliomas, and parathyroid adenomas). CCK-A receptors were expressed rarely in tumors except in gastroenteropancreatic tumors (38%), meningiomas (30%), and some neuroblastomas (19%). The identified CCK-A and CCK-B receptors were specific and of high affinity in the subnanomolar range. The rank order of potency of various CCK analogues was: sulfated CCK-8 = L-364,718 >> nonsulfated CCK-8 = L-365,260 > or = gastrin for CCK-A receptors and sulfated CCK-8 > gastrin = nonsulfated CCK-8 > L-365,260 > L-364,718 for CCK-B receptors. CCK-B receptors could also be selectively and specifically labeled with a newly designed nonsulfated 125I-(D-Tyr-Gly, Nle28,31)-CCK 26-33. Gastrin mRNA measured by in situ hybridization was present in most CCK-B receptor-positive small cell lung cancers, breast tumors, and ovarian tumors, representing the molecular basis of a possible autocrine growth regulation of these tumors. Gastrin and CCK mRNAs were lacking in medullary thyroid cancers. Thus, these results may have pathogenic, diagnostic, differential diagnostic, and therapeutic implications.

Topics: Autoradiography; Breast Neoplasms; Carcinoma, Small Cell; Cholecystokinin; Female; Gastrins; Humans; Lung Neoplasms; Neoplasms; Neuroendocrine Tumors; Ovarian Neoplasms; Receptor, Cholecystokinin A; Receptor, Cholecystokinin B; Receptors, Cholecystokinin; Sincalide; Thyroid Neoplasms