Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10415 (Bcl-2)
 33,771 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the expression of the apoptosis-suppressing protein Bcl-2 in head and neck neoplasm and the relationship between Bcl-2 and p53 oncoprotein, 90 malignant tumours and 20 benign diseases were studied with immunohistochemical LSAB(labeled streptavidin biotin) method. The results indicated that 48.9% (44/90) cases of head and neck malignant tumours were Bcl-2 positive, and all benign diseases were negative. The expression rate of Bcl-2 in head and neck squamous carcinoma (59.6%) was obviously higher than adenocarcinoma (24.8%), undifferentiated tumour (33.3%) and malignant lymphoma (P < 0.05). The expression rate of Bcl-2 in p53-positive tumours was significantly higher in p53-negative neoplasm. The positive rate of Bcl-2 oncoprotein was not connected with clinical stage and pathological grade. The positive staining intensity was significantly related with clinical stage. This study suggested that Bcl-2 oncoprotein may play an important role in the development of head and neck tumour.
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PMID:[Bcl-2 oncoprotein expression in head and neck malignant neoplasm]. 1118 50

Oral squamous cell carcinoma (OSCC) is one of the most common types of head and neck neoplasm. Down-regulation of hsa-microRNA-378 (miR-378) has been proved in OSCC tissues, suggesting that miR-378 might play crucial roles in the progression of OSCC. The present study aimed to evaluate the effect of miR-378-3p/5p on the proliferation and apoptosis of OSCC in vitro and in vivo. According to the results, lentivirus-mediated overexpression of miR-378 lowered the colony formation efficiency, blocked cell cycle progression, and decreased the percentage of Ki-67 positive cells, whereas knockdown of miR-378-3p/5p led to the opposite results. Furthermore, the apoptosis of OSCC cells was induced by the overexpression of miR-378 as evidenced by decreasing Bcl-2/Bax ratio, increasing cleaved caspase-9, cleaved caspase-3, and cleaved PARP levels, and promoting the release of cytochrome c into the cytoplasm. However, the above results were reversed by miR-378-3p/5p silencing. In addition, the overexpression of miR-378 inhibited the activation of PI3K/AKT signalling pathway. Conversely, miR-378-3p/5p knockdown resulted in the inactivation of PI3K/AKT signalling pathway. Mechanically, we validated that miR-378-3p/5p could target kallikrein-related peptidase 4 (KLK4), and enforced overexpression of KLK4 counteracted miR-378 overexpression-induced apoptosis. Finally, tumourigenesis in nude mice was suppressed by the overexpression of miR-378, which was promoted by miR-378-3p/5p silencing. Taken together, these results suggest that miR-378 may be a potential target in the diagnoses and treatment of OSCC.
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PMID:MicroRNA-378-3p/5p represses proliferation and induces apoptosis of oral squamous carcinoma cells via targeting KLK4. 3186 42