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AIM To evaluate the role of RARα gone in mediating thegrowth inhibitory effect of all-trans retinoic acid(ATRA)on gastric cancer cells.METHODS The expression levels of retinoic acidreceptors(PARs)in gastric cancer cells were detected byNorthern blot.Transient transfection and chlorophenicolacetyl transferase(CAT)assay were used to show thetranscriptional activity of β retinoic acid response element(βPARE)and AP-1 activity.Cell growth inhibition wasdetermined by MTT assay and anchorage-independentgrowth assay,respectively.Stable transfection wasperformed by the method of Lipofectamine,and the cellswere screened by G418.RESULTS ATRA could induce expression level of RARα inMGC80-3,BGC-823 and SGC-7901 cells obviously,resulting in growth inhibition of these cell lines.Aftersense RARα gone was transfected into MKN-45 cells thatexpressed rather low level of RARα and could not beinduced by ATPA,the cell growth was inhibited by ATPAmarkedly.In contrast,when antisense RARα gone wastransfected into BGC-823 cells,a little inhibitory effect byATPA was seen,compared with the parallel BGC-823cells.In transient transfection assay,ATPA effectivelyinduced transcriptional activity of βRARE in MGC80-3,BGC-823,SGC-7902 and MKN/RARα cell lines,but not inMKN-45 and BGC/aRARα cell lines.Similar results wereobserved in measuring anti-AP-1 activity by ATPA in thesecancer cell lines.CONCLUSION ATRA inhibits the growth of gastric cancercells by up-regulating the level of RARα; RARα is themajor mediator of ATRA action in gastric cancer cells;andadequate level of RARα is required for ATRA effect ongastric cancer cells.
AIM To evaluate the role of RARα gone in mediating the growth inhibitory effect of all-trans retinoic acid(ATRA) on gastric cancer cells.METHODS The expression levels of retinoic acidreceptors(PARs)in gastric cancer cells were detected by Northern blot.Transient transfection and chlorophenicolacetyl Transferase(CAT) assay were used to show thetranscriptional activity of β retinoic acid response element(βPARE) and AP-1 activity.Cell growth inhibition was determined by MTT assay and anchorage-independent growth assay,respectively.Stable transfection wasperformed by the method of Lipofectamine, And the cellswere screened by G418.RESULTS ATRA could induce expression level of RARα inMGC80-3,BGC-823 and SGC-7901 cells obviously,resulting in growth inhibition of these cell lines.Aftersense RARα gone was transfected into MKN-45 cells thatexpressed rather Low level of RARα and could not beinduced by ATPA, the cell growth was inhibited by ATPAmarkedly.In contrast, when antisense RARα gone wastransf Ected into BGC-823 cells, a little inhibitory effect by ATPA was seen,compared with the parallel BGC-823 cells. In transient transfection assay,ATPA validinduced transcriptional activity of βRARE in MGC80-3, BGC-823, SGC-7902 and MKN/RARα Cell lines, but not inMKN-45 and BGC/aRARα cell lines.Similar results wereobserved in measuring anti-AP-1 activity by ATPA in these cancer cell lines.CONCLUSION ATRA inhibits the growth of gastric cancer cells by up-regulating the level of RARα; RARα is themajor mediator of ATRA action in gastric cancer cells; andadequate level of RARα is required for ATRA effect ongastric cancer cells.