Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
 11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thyroid cancer is well known to be hormone sensitive as well as breast cancer, prostatic cancer, and endometrial cancer of the uterus. Various experimental results suggest that the growth regulation for thyroid cancer, as well as the normal thyroid gland, appears to depend upon the TSH (Thyroid stimulating hormone) receptor on cell membranes. Differentiated thyroid carcinoma cells possess TSH receptor, although anaplastic carcinoma cells do not; therefore suppression therapy of TSH with thyroid hormone is considered to be effective against differentiated thyroid carcinoma. It has been recognized that some recurrent differentiated thyroid cancers cause regression in size in response to treatment with thyroid hormone. But the administration of the thyroid hormone after the operation for the differentiated thyroid carcinoma does not necessarily enhance the survival rate. To analyze the difference in survival rate is very difficult because of the excellent survival rate of thyroid cancer patients after the operation. It is hoped that further clinical study and laboratory investigation about suppression in adjuvant therapy for differentiated thyroid cancer will give us a conclusive answer.
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PMID:[The effect of thyroid hormone on the growth of thyroid cancer]. 268 57

Thyroid dysfunction is involved in several types of carcinoma. Hypothyroidism is one of the most common medical morbidities among patients with endometrial cancer; however, the related mechanism is unclear. Among the risk factors related to endometrial cancer, hypothyroidism interacts with metabolic syndrome, polycystic ovarian syndrome and infertility or directly acts on the endometrium itself, which may influence the development and progression of endometrial cancer. We summarize recent studies on the relationship between hypothyroidism and endometrial cancer and its risk factors to provide references for basic research as well as for clinical treatment and prognostic evaluation.
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PMID:Relationship between Hypothyroidism and Endometrial Cancer. 3070 78

Background: MicroRNA-589-5p (miR-589-5p) has been recently reported to be aberrantly regulated in hepatocellular carcinoma, but its functional role and molecular mechanisms still remains unknown in the endometrial carcinoma (EC) as one of the most common female malignancies. Methods: EC tissues and adjacent tissues were collected to determine the expression of miR-589-5p and thyroid receptor interacting protein 6 (TRIP6) using quantitative real time-PCR. Subsequently, two EC cell lines HEC-1B and AN3CA were transfected with miR-589-5p to achieve miR-589-5p overexpression. Using Cell Counting Kit-8 (CCK-8), a wound healing assay and the Transwell assay, we analyzed cell proliferation, migration and invasion. Dual-luciferase reporter assay confirmed that thyroid receptor interacting protein 6 (TRIP6) was a direct target of miR-589-5p. Results: We first observed that miR-589-5p was down-regulated in EC tissues compared with normal endometrial tissues. MiR-589-5p overexpression significantly suppressed EC cell proliferation, migration and invasion. Thyroid receptor interacting protein 6 (TRIP6) was a direct target of miR-589-5p. Besides, TRIP6 knockdown presented similar effects on cell proliferation, migration and invasion to miR-589-5p overexpression. Furthermore, TRIP6 knockdown efficiently enhanced the effects of miR-589-5p on the above cellular function. Moreover, miR-589-5p up-regulated E-cadherin expression, but down-regulated N-cadherin and Vimentin by targeting TRIP6. Conclusions: In summary, miR-589-5p might function as a tumor suppressor by targeting TRIP6, which will provide new insights into the molecular mechanism underlying the development of EC.
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PMID:Targeting Thyroid Receptor Interacting Protein 6 by MicroRNA-589-5p Inhibits Cell Proliferation, Migration, and Invasion in Endometrial Carcinoma. 3142 77