Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1384489 (Scratch)
 395 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The protein tyrosine phosphatase 1B (PTP1B) is an important regulator of metabolism. The relationship between PTP1B and tumors is quite complex. The purpose of this study is to explore the expression pattern and role of PTP1B in breast cancer. The expression of PTP1B was detected in 67 samples of breast cancer tissue by Western blot. Cell growth assay, Transwell migration assay, and Scratch motility assay were used to examine the proliferation and migration of MCF-7 with and without PTP1B. The total levels and phosphorylated levels of signal transduction and activator of transcription 3 (STAT3) and the expression of C-C motif chemokine ligand 5 (CCL5) were also examined by Western blot. PTP1B was overexpressed in over 70% of breast cancer tissues, correlating with patients with estrogen receptor (ER)-negative, progesterone receptor (PR)-negative, and human epidermal growth factor receptor 2 (HER2)-positive tumors. The data also showed that both tumor size and lymph node metastasis were significantly higher in patients with a higher level of PTP1B. The proliferation and migration of MCF-7 cells were found to be inhibited after knocking down the gene of PTP1B. Our data also showed that PTP1B could up-regulate the dephosphorylated level of STAT3, which could increase the expression of CCL5. These phenomena indicated that PTP1B may play a crucial role in the development of breast cancer.
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PMID:Protein tyrosine phosphatase 1B expression contributes to the development of breast cancer. 2837 71

The chemokine CXCL10 and its receptor CXCR3 have been demonstrated to be implicated in cancer cell proliferation and metastasis. CXCR3 has three splice variants: CXCR3A, CXCR3B and CXCR3-alt. CXCR3A and B serve multiple roles in the growth and invasiveness of a number of cancer types. However, the roles of CXCR3 isoforms in colorectal cancer (CRC) cells remain unclear. In the current study, the effects of CXCL10 and CXCR3 isoforms on proliferation and invasion of CRC cells was examined. Proliferation and invasiveness of the CRC cell line HCT116, which were transfected with CXCR3A or CXCR3B in the presence of CXCL10, were evaluated in vitro using MTT, scratch wound healing and transwell assays. MTT assay indicated that regardless of the presence or absence of CXCL10, the proliferative ability of CXCR3A-transfected HCT116 cells was enhanced compared with blank and mock cells. Scratch wound healing and transwell assays indicated that invasiveness of CXCR3A-transfected cells was greater compared with blank and mock cells. However, HCT116 cells transfected with CXCR3B did not exhibit changes in their proliferative or invasive ability. mRNA expression of MMP9, which is associated with signaling downstream of the CXCL10/CXCR3A pathway, was increased 4-fold in CXCR3A-transfected HCT116 cells compared with control cells. The results of the present study indicated that CXCL10-enhanced proliferation and invasiveness of the CRC cell line HCT116 was likely mediated by CXCR3A, but not by CXCR3B.
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PMID:C-X-C motif receptor 3A enhances proliferation and invasiveness of colorectal cancer cells, and is mediated by C-X-C motif ligand 10. 3219 50