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PubMed | Tianjin Baodi Hospital Tianjin 301800 and Tianjin Hospital Tianjin 300211
Type: Journal Article | Journal: International journal of clinical and experimental pathology | Year: 2015

Recent data strongly suggest the important role of miRNAs in various cancer-related processes. Osteosarcoma is the most common type of primary malignant bone tumor and is characterized by complex genetic changes and resistance to conventional treatments. In this study, the role of miRNA-15a (miR-15a) in the progression and metastasis of osteosarcoma was investigated. The result demonstrated that the expression of miR-15a was down-regulated in osteosarcoma tissues and cell lines as compared with that in adjacent non-neoplastic bone tissues and the osteoblastic cell line. In functional assays, miR-15a inhibited cell proliferation, migration and invasion in U2OS and MG-63 cells. Meanwhile, bioinformatic analysis combined with experimental confirmation demonstrated that tumor necrosis factor; -induced protein 1 (TNFAIP1) gene is a potential target of miR-15a and can be directly regulated by miR-15a. Down-regulation of TNFAIP1 induced effects on osteosarcoma cell lines similar to those induced by miR-15a. Taken together, these data suggest that miR-15a may act as a tumor suppressor, which is commonly down-regulated in both osteosarcoma tissues and cells. TNFAIP1 plays an important role in mediating miR-15a dependent biological functions in osteosarcoma. Reintroduction of miR-15a may be a novel therapeutic strategy by down-regulating TNFAIP1 expression.


PubMed | Tianjin Hospital Tianjin 300211, Tianjin Medical University and Tianjin Institute of Urology Tianjin 300211
Type: Journal Article | Journal: International journal of clinical and experimental pathology | Year: 2015

MicroRNAs (miRNAs) are known to function as negative gene regulators. Recently, miRNAs have been shown to regulate immunity processes; however, the mechanism is unclear. The role of microRNA-214 (miR-214) in dendritic cell (DC) maturation has not been investigated. We found that the miR-214 level was correlated with the maturation of DCs and inflammatory cytokine secretion, as depressed miR-214 levels induced DC tolerance. We also identified -catenin as a target gene of miR-214 and demonstrated its association with Treg cell differentiation. MiR-214 regulates gene expression by binding to the 3UTR of -catenin. The results suggest that -catenin is a critical regulator of tolerance in DCs via miR-214. The expression of miR-214 could be a potential therapeutic strategy in organ transplantation or autoimmunity patients.


PubMed | Tianjin Hospital Tianjin 300211, The Affiliated Hospital of CPAP of Logistic College Tianjin 300162 and Tianjin Academy of Traditional Chinese Medicine Affiliated Hospital Tianjin 300120
Type: Journal Article | Journal: International journal of clinical and experimental medicine | Year: 2016

Abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) and the stimulation of platelet-derived growth factor (PDGF)-BB play major pathological processes involved in the development of cardiovascular diseases. As a result, the use of anti-proliferative and anti-migratory agents for VSMCs offers promise for the treatment of vascular disorders. Myricitrin is a naturally occurring phenolic compound which possesses antioxidant and anti-inflammatory activity. In this study, we investigate the inhibitory effect of myricitrin on PDGF-BB-induced VSMCs proliferation and migration. In accordance with these findings, myricitrin induced the arrest of cell cycle progression at G0/G1 phase. Myricitrin also decreased the expressions of G0/G1 specific regulatory proteins including cyclin D1, cyclin-dependent kinases (CDK) 4, cyclin E and CDK2, as well as increased the expression of p21 in PDGF-BB-induced VSMCs. Moreover, myricitrin inhibited PDGF-BB-induced phosphorylation of PDGFR, Akt and Erk1/2. These results suggest that myricitrin plays an important role in prevention of VSMCs proliferation and migration through the G0/G1 cell cycle arrest by PDGF signaling pathway. Thus, myricitrin is effective in reducing atherosclerotic process by blocking proliferation of VSMCs.


PubMed | Tianjin Hospital Tianjin 300211 and Tianjin Medical University
Type: Journal Article | Journal: International journal of clinical and experimental pathology | Year: 2016

Tubeimoside-1 (TBMS1) is considered to have anti-tumor properties. However, the role of TBMS1 on human colorectal cancer (CRC) is still unclear. Therefore, in this study, we investigated the role of TBMS1 on human CRC and explored the underlying mechanism. The cell proliferation of CRC cells was detected by MTT assay. Cell migration and invasion were assessed by Boyden chamber assay, and the involvement of molecular mechanisms was examined by western blot. In this study, we found that TBMS1 inhibited the proliferation, migration/invasion of CRC cells, and it reduced -catenin expression in CRC cells. Furthermore, overexpression of -catenin rescued TBMS1-induced proliferation and invasion inhibition, and knockdown of -catenin potentiated TBMS1-induced proliferation and invasion inhibition. Taken together, our results demonstrate that TBMS1 inhibited CRC cell proliferation and invasion via suppressing the Wnt/-catenin signaling pathway. Therefore, TBMS1 may represent a chemopreventive and/or therapeutic agent in the prevention of CRC.


PubMed | Tianjin Hospital Tianjin 300211 and Tianjin Medical University
Type: Journal Article | Journal: International journal of clinical and experimental pathology | Year: 2015

Colorectal cancer is one of the leading causes of cancer related deaths worldwide. Cullin 4B (CUL4B) is over-expressed in diverse cancer types. However, the function and precise molecular mechanism of CUL4B in colorectal cancer remains largely unknown. Therefore, in this study, we examined the expression of CUL4B in colorectal cancer cell lines and its effects on cellular proliferation and apoptosis, and the underlying mechanism was also explored. Our results showed that CUL4B was significantly overexpressed in colorectal cancer cell lines. Silencing CUL4B obviously inhibited proliferation and tumorigenicity of colorectal cancer cells both in vitro and in vivo, and it also promoted the apoptosis of colorectal cancer cells. Moreover, knockdown of CUL4B inhibited the expression of -catenin, cyclin D1 and c-Myc in colorectal cancer cells. Taken together, these results showed that knockdown of CUL4B inhibit proliferation and promotes apoptosis of colorectal cancer cells through suppressing the Wnt/-catenin signaling pathway. Therefore, CUL4B may represent a novel therapeutic target for colorectal cancer treatment.

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