Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1864663 (HCC)
 2,985 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Octamer binding transcription factor 4 (OCT4), a key transcription factor required to maintain self-renewal and pluripotency of human and mouse embryonic stem cells, has been recently identified to be associated with tumorigenesis and malignant transformation of many types of cancers. This study was to determine the roles of OCT4 in HCC recurrence and their impact on the clinical outcome of HCC patients. Western blot and immunohistochemical stains were used to detect the expression of OCT4 protein in 152 HCC tissues and 40 cirrhosis tissues, as well as in 6 human HCC cell lines and normal hepatocytes. OCT4 expression in HCC cell lines and tumor tissues was higher than in normal hepatocytes and cirrhosis tissues. Overexpression of OCT4 was significantly associated with low differentiation and tumor recurrence. Patients with elevated expression of OCT4 protein usually carried a poor overall survival and high recurrence rate. Multivariate analysis showed that OCT4 expression was an independent predictive factor for HCC patients survival. OCT4 might serve as a promising biomarker for the diagnosis of highly recurrent cases of HCC and could be used as a valuable indicator for predicting the prognosis of HCC.
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PMID:Increased expression of OCT4 is associated with low differentiation and tumor recurrence in human hepatocellular carcinoma. 2282 46

Triple-negative breast cancer (TNBC) has the poorest prognosis among all types of breast cancer and there is yet no effective therapy. Chemotherapy is the traditional standard of care for patients with TNBC; however, treatment of TNBC with chemotherapy may lead to the enrichment of cancer stem cells (CSCs), which exhibitan enhanced capacity for self-renewal, tumor initiation and metastasis. The present study demonstrated that bufalin, a small molecular compound used in traditional Chinese medicine, exerted anticancer effects on a wide range of cancer cell lines, inhibited cell proliferation through inducing G2/M cell cycle arrest, and triggered apoptosis in the TNBC cell lines MDA-MB-231 and HCC-1937. Consistently, bufalin markedly suppressed TNBC growth in a cell line-derived xenograft model. More importantly, unlike common chemotherapeutic drugs, bufalin reduced the stemness of TNBC stem cells. A mechanistic study suggested that bufalin may suppress the proliferation of TNBC stem cells by inhibiting the expression of octamer-binding transcription factor 4 (OCT4) and sex determining region Y-box 2 (SOX2) in MDA-MB-231 and HCC-1937 cells. These results indicated that bufalin may hold promise as a therapeutic agent in TNBC, and its effects may be mediated through the SOX2/OCT4 axis.
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PMID:Bufalin attenuates triple-negative breast cancer cell stemness by inhibiting the expression of SOX2/OCT4. 3293 38

The oncogene yes-associated protein (YAP) controls liver tumor initiation and progression via cell extrinsic functions by creating a tumor-supporting environment in conjunction with cell autonomous mechanisms. However, how YAP controls organization of the microenvironment and in particular the vascular niche, which contributes to liver disease and hepatocarcinogenesis, is poorly understood. To understand heterotypic cell communication, we dissected murine and human liver endothelial cell (EC) populations into liver sinusoidal endothelial cells (LSECs) and continuous endothelial cells (CECs) through histo-morphological and molecular characterization. In YAPS127A-induced tumorigenesis, a gradual replacement of LSECs by CECs was associated with dynamic changes in the expression of genes involved in paracrine communication. The formation of new potential communication hubs connecting CECs and LSECs included the hepatocyte growth factor (Hgf)/c-Met signaling pathway. In hepatocytes and tumor cells, YAP/TEA domain transcription factor 4 (TEAD4)-dependent transcriptional induction of osteopontin (Opn) stimulated c-Met expression in EC with CEC phenotype, which sensitized these cells to the pro-migratory effects of LSEC-derived Hgf. In human HCC, the presence of a migration-associated tip-cell signature correlated with poor clinical outcome and the loss of LSEC marker gene expression. The occurrence of c-MET-expressing CEC in human liver cancer samples was confirmed at the single cell level. In summary, YAP-dependent changes of the liver vascular niche comprise the formation of heterologous communication hubs in which tumor cell-derived factors modify the crosstalk between LSECs and CECs via the HGF/c-MET axis.
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PMID:YAP orchestrates heterotypic endothelial cell communication via HGF/c-MET signaling in liver tumorigenesis. 3308 21