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)

Sex determining region Y-box protein 12 (SOX12) plays an important role in the tumorigenesis of hepatocellular carcinoma. The involvement of SOX12 in human lung cancer is not well-understood. The aim of the current study was to explore the expression pattern and function of SOX12 in lung cancer. SOX12 expression in lung cancer tissues was elevated as assessed by analyzing The Cancer Genome Atlas (TCGA) lung cancer cohort and real-time PCR data of our own cohort. We found that SOX12 mRNA expression was up-regulated in 83.3% (75/90) of the lung cancer tissues in comparison with paired normal tissues. Moreover, high SOX12 expression predicted reduced overall survival. We also found that knockdown of SOX12 in SPC-A-1 and A549 cells impaired lung cancer cell proliferation, migration and invasion in vitro, but promoted lung cancer cell apoptosis. In vivo tumorigenesis experiments showed that inhibition of SOX12 expression significantly suppressed the growth of xenograft tumors. Finally, the mRNA and protein levels of cell growth (PCNA and Cyclin E), apoptosis (Bcl-2 and Bax), invasion (matrix metalloproteinase-9) and epithelial-mesenchymal transition (EMT; Twist1 and E-cadherin) related moderators were affected by SOX12 knockdown. Chromatin immunoprecipitation assays showed that Cyclin E and Twist1 were direct transcriptional targets of SOX12. Taken together, our study suggests that SOX12 functions as an oncogenic molecule during the development of human lung cancer.
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PMID:Knockdown of SOX12 expression inhibits the proliferation and metastasis of lung cancer cells. 2897 76

Osteosaroma (OS) is a primary bone malignancy and is associated with high morbidity. Sex determining region Y-box 18 (SOX18) is identified overexpressed in OS. However, the molecular mechanism underlying the biological function of SOX18 in OS is still unclear. The aim of the current study was to determine the SOX18 expression in patients with OS and its effect on tumor cell malignant phenotypes. Our results showed that SOX18 was overexpressed in OS patients from both E-MEXP-3628 database and independent samples from our hospital and in OS cell lines. SOX18 silencing significantly induced G0-G1 phase cell cycle arrest and apoptosis and inhibited U-2OS cell migration and invasion and cell growth both in vitro and in vivo. However, SOX18 overexpression remarkably promoted 143B cell proliferation, migration and invasion and inhibited cell cycle arrest and apoptosis. The protein expression levels of p53, p21, Bax, Bcl-2, and Caspase-3 were also regulated by SOX18. Moreover, SOX18 was found negative correlated with the expression of HERC1, HER2, HERC3, HERC4, HERC5, and HERC6 in OS patients and in OS cells, with the most significant correlation detected in HERC2 expression, which was following found interacted with SOX18 in OS cells. Taken together, our results suggest that SOX18 is overexpressed in OS and plays an important role in proliferation, apoptosis, migration and invasion of OS cells, and may provide a novel and promising thera-peutic strategy for OS.
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PMID:Heterogeneous expression and biological function of SOX18 in osteosaroma. 2926 13