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RISS 인기검색어
- 검색키워드
- 저자 : Xumin Pian (검색결과 4 건)
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Establishment and Characterization of Three Immortal Bovine Muscular Epithelial Cell Lines
진선,이중섭,곽성욱,이수연,정지은,김태경,Chenxiong Xu,홍종산,Zhehu Li,김선명,Xumin Pian,이동희,윤종택,유승권,최윤재,김형기 한국분자세포생물학회 2006 Molecules and cells Vol.21 No.1
We have established three immortal bovine muscularepithelial (BME) cell lines, one spontaneously immortalized(BMES), the second SV40LT-mediated (BMEV)and the third hTERT-mediated (BMET). The morphologyof the three immortal cell lines was similar tothat of early passage primary BME cells. Each of theimmortal cell lines made cytokeratin, a typical epithelialmarker. BMET grew faster than the other immortallines and the BME cells, in 10% FBS-DMEM medium,whereas neither the primary cells nor the threeimmortal cell lines grew in 0.5% FBS-DMEM. Theprimary BME cells and the immortal cell lines, withthe exception of BMES, made increasing amounts ofp53 protein when treated with doxorubicin, a DNAdamaging agent. On the other hand, almost half of thecells in populations of the three immortal cell linesmay lack p16INK4a regulatory function, compared toprimary BME cells that were growth arrested by enforcedexpression of p16INK4a. In soft-agar assays, theprimary cells and immortal cell lines proved to be lesstransformed in phenotype than HeLa cells. The threeimmortal epithelial-type cell lines reported here arethe first cell lines established from muscle tissue ofbovine or other species.
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백삼열,Xun Jin,Young-Woo Sohn,Jun-Kyum Kim,김성학,Jinlong Yin,Xumin Pian,김성찬,남도현,최윤재,김형기 한국분자세포생물학회 2011 Molecules and cells Vol.31 No.1
Telomerase reverse transcriptase (TERT), the catalytic subunit of the enzyme telomerase, is robustly expressed in cancer cells. TERT enables cells to avoid chromosome shortening during repeated replication by maintaining telomere length. However, several lines of evidence indi-cate that many cancer cells exhibit shorter telomere length than normal tissues, implying an additional function of TERT in tumor formation and progression. Here, we report a telomerase activity-independent function of TERT that induces cancer stemness in glioma cells. Overexpression of TERT712, a telomerase activity-deficient form of TERT, in U87MG cells promoted cell self-renewal in vitro, and induced EGFR expression and formation of gliomas exhibiting cellular heterogeneity in vivo. In patients with gliobla-stoma multiforme, TERT expression showed a high corre-lation with EGFR expression, which is closely linked to the stemness gene signature. Induction of differentiation and TERT-knockdown in glioma stem cells led to a marked reduction in EGFR expression, cancer stemness, and anti-cancer drug resistance. Together, our findings indicate that TERT plays a crucial role in tumor progres-sion by promoting cancer stemness through expression of EGFR.
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Jin, Xun,Beck, Samuel,Sohn, Young-Woo,Kim, Jun-Kyum,Kim, Sung-Hak,Yin, Jinlong,Pian, Xumin,Kim, Sung-Chan,Choi, Yun-Jaie,Kim, Hyung-Gee Korean Society for Biochemistry and Molecular Bion 2010 Experimental and molecular medicine Vol.42 No.8
Although human telomerase catalytic subunit (TERT) has several cellular functions including telomere homeostasis, genomic stability, cell proliferation, and tumorigenesis, the molecular mechanism underlying anti-apoptosis regulated by TERT remains to be elucidated. Here, we show that ectopic expression of TERT in spontaneously immortalized human fetal fibroblast (HFFS) cells, which are a telomerase- and p53-positive, leads to increases of cell proliferation and transformation, as well as a resistance to DNA damage response and inactivation of p53 function. We found that TERT and a mutant TERT (no telomerase activity) induce expression of basic fibroblast growth factor (bFGF), and ectopic expression of bFGF also allows cells to be resistant to DNA-damaging response and to suppress activation of p53 function under DNA-damaging induction. Furthermore, loss of TERT or bFGF markedly increases a p53 activity and DNA-damage sensitivity in HFFS, HeLa and U87MG cells. Therefore, our findings indicate that a novel TERT-bFGF axis accelerates the inactivation of p53 and consequent increase of resistance to DNA-damage response.
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Establishment of Immortal Swine Kidney Epithelial Cells
Kwak, Sungwook,Jung, Ji-Eun,Jin, Xun,Kim, Sun-Myung,Kim, Tae-Kyung,Lee, Joong-Seob,Lee, Soo-Yeon,Pian, Xumin,You, Seungkwon,Kim, Hyunggee,Choi, Yun-Jaie Taylor Francis 2006 Animal biotechnology Vol.17 No.1
<P> Using normal swine kidney epithelial (SKE) cells that were shown to be senescent at passages 12 to 14, we have established one lifespan-extended cell line and two lifespan-extended cell lines by exogenous introduction of the human catalytic subunit of telomerase (hTERT) and simian virus 40 large T-antigen (SV40LT), all of which maintain epithelial morphology and express cytokeratin, a marker of epithelial cells. SV40LT- and hTERT-transduced immortal cell lines appeared to be smaller and exhibited more uniform morphology relative to primary and spontaneously immortalized SKE cells. We determined the in vitro lifespan of primary SKE cells using a standard 3T6 protocol. There were two steps of the proliferation barrier at 12 and 20, in which a majority of primary SKE cells appeared enlarged, flattened, vacuolated, and &bgr;-galactosidase-positive, all phenotypical characteristics of senescent cells. Lifespan-extended SKE cells were eventually established from most of the cellular foci, which is indicative of spontaneous cellular conversion at passage 23. Beyond passage 25, the rate of population doubling of the established cells gradually increased. At passage 30, immortal cell lines grew faster than primary counterpart cells in 10% FBS-DMEM culture conditions, and only SV40LT-transduced immortal cells grew faster than primary and other SKE immortal cells in 0.5% FBS-DMEM. These lifespan-extended SKE cell lines failed to grow in an anchorage-independent manner in soft-agar dishes. Hence, three immortalized swine kidney epithelial cells that are not transformed would be valuable biological tools for virus propagation and basic kidney epithelial cell research.</P>
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