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10.18632/oncotarget.10407

http://scihub22266oqcxt.onion/10.18632/oncotarget.10407
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suck abstract from ncbi


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pmid27391336
      Oncotarget 2017 ; 8 (9 ): 14479-14486
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  • Long non-coding RNA SPRY4-IT1 pormotes colorectal cancer metastasis by regulate epithelial-mesenchymal transition #MMPMID27391336
  • Shen F ; Cai WS ; Feng Z ; Chen JW ; Feng JH ; Liu QC ; Fang YP ; Li KP ; Xiao HQ ; Cao J ; Xu B
  • Oncotarget 2017[Feb]; 8 (9 ): 14479-14486 PMID27391336 show ga
  • Colorectal cancer (CRC) remains one of the most common cancers worldwide. Increasing evidence indicates that SPRY4 intronic transcript 1 (SPRY4-IT1) regulate cell growth, differentiation, apoptosis, and cancer progression. However, the expression and function of SPRY4-IT1 in the progression of CRC remains largely unknown. Here, we reported that SPRY4-IT1 was upregulated in CRC. Increased SPRY4-IT1 expression in CRC was associated with larger tumor size and higher clinical stage. In vitro experiments revealed that SPRY4-IT1 knockdown significantly inhibited CRC cell proliferation by causing G1 arrest and promoting apoptosis, whereas SPRY4-IT1 overexpression promoted cell proliferation. Further functional assays indicated that SPRY4-IT1 overexpression significantly promoted cell migration and invasion by regulate the epithelial-mesenchymal transition (EMT). Taken together, our study demonstrates that SPRY4-IT1 could act as a functional oncogene in CRC, as well as a potential therapeutic target to inhibit CRC metastasis.
  • |*Cell Movement [MESH]
  • |*Gene Expression Regulation, Neoplastic [MESH]
  • |Apoptosis [MESH]
  • |Biomarkers, Tumor/*genetics [MESH]
  • |Blotting, Western [MESH]
  • |Cell Proliferation [MESH]
  • |Colorectal Neoplasms/genetics/*secondary [MESH]
  • |Epithelial-Mesenchymal Transition/*genetics [MESH]
  • |Humans [MESH]
  • |RNA, Long Noncoding/*genetics [MESH]
  • |RNA, Messenger/genetics [MESH]
  • |Real-Time Polymerase Chain Reaction [MESH]
  • |Reverse Transcriptase Polymerase Chain Reaction [MESH]


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