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      Inhibition of Cervical Cancer Cell Growth by Gene Silencing of HPV16 E6 Induced by Short-interfering RNA

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      https://www.riss.kr/link?id=A103913795

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      다국어 초록 (Multilingual Abstract) kakao i 다국어 번역

      The Human Papilloma Virus (HPV) infection has been strongly associated with pathogenesis of uterine cervix carcinoma. HPV type 16, a causative agent of uterine cervix carcinoma, encodes the E6 and E7 oncogenes, expression of which is pivotal for malignant transformation and maintenance of malignant phenotypes. To develop a gene therapy for HPV-related carcinoma, We investigated the effect of E6 short-interfering RNA (E6 siRNA) on the expression of this oncogene and on the growth of HPV 16-related uterine cervix carcinoma cells. SiHa cells, a uterine cervix carcinoma cell line, which contain a single copy of HPV 16 integrated in the chromosome and express the E6 and E7 oncogenes. Before 24 hr of transfection, cells were seeded and transfected with control plasmid or E6 siRNA-expressing plasmid. The mRNA was analysed by reverse transcriptase polymerase chain reaction (RT- PCR). The cell growth rate was investigated by MTT method. The E6 mRNA level in SiHa cells was decreased in HPV 16 E6 siRNA-expression vector transfected cells and a decrease in the growth of these cells was also observed. From these results. it is evident that E6 siRNA played a role in suppression of growth of SiHa cells and has a fair chance as a candidate for gene specific therapy for HPV related uterine cervix carcinoma.
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      The Human Papilloma Virus (HPV) infection has been strongly associated with pathogenesis of uterine cervix carcinoma. HPV type 16, a causative agent of uterine cervix carcinoma, encodes the E6 and E7 oncogenes, expression of which is pivotal for malig...

      The Human Papilloma Virus (HPV) infection has been strongly associated with pathogenesis of uterine cervix carcinoma. HPV type 16, a causative agent of uterine cervix carcinoma, encodes the E6 and E7 oncogenes, expression of which is pivotal for malignant transformation and maintenance of malignant phenotypes. To develop a gene therapy for HPV-related carcinoma, We investigated the effect of E6 short-interfering RNA (E6 siRNA) on the expression of this oncogene and on the growth of HPV 16-related uterine cervix carcinoma cells. SiHa cells, a uterine cervix carcinoma cell line, which contain a single copy of HPV 16 integrated in the chromosome and express the E6 and E7 oncogenes. Before 24 hr of transfection, cells were seeded and transfected with control plasmid or E6 siRNA-expressing plasmid. The mRNA was analysed by reverse transcriptase polymerase chain reaction (RT- PCR). The cell growth rate was investigated by MTT method. The E6 mRNA level in SiHa cells was decreased in HPV 16 E6 siRNA-expression vector transfected cells and a decrease in the growth of these cells was also observed. From these results. it is evident that E6 siRNA played a role in suppression of growth of SiHa cells and has a fair chance as a candidate for gene specific therapy for HPV related uterine cervix carcinoma.

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      참고문헌 (Reference)

      1 Hussain SP, "p53 mutation spectrum and load: the generation of hypotheses linking the exposure of endogenous or exogenous carcinogens to human carcinoma" 428 : 23-32, 1999

      2 Havre PA, "p53 inactivation by HPV16 E6 results in increased mutagenesis in human cells" 55 : 4420-4424, 1995

      3 Quintanilla-Martinez L, "p53 Mutations in nasal natural killer / T-cell lymphoma from Mexico:association with large cell morphology and advanced disease" 159 : 2095-2105, 2001

      4 Plasterk RH, "The silence of the genes" 10 : 562-567, 2000

      5 Schwarz E., "Stremalau A zur Hasusen H. Structure and transcription of human papilloma virus sequences in utrine cervix carcinoma cells" 314 : 111-114, 1985

      6 Gitlin L, "Short interfering RNA confers intracellular antiviral immunity in human cells" 418 : 430-434, 2002

      7 Matsukura T, "Relationships between 80 human papilloma virus genotypes and different grades of cervical intraepithelial neoplasia: association and causality" 283 (283): 39-47, 2001

      8 Hashiguchi Y, "Relationship between HPV typing and the status of G2 cell cycle regulators in cervical neoplasia" 12 : 587-591, 2004

      9 Taylor WR, "Regulation of the G2 / M transition by p53" 20 : 1803-1815, 2001

      10 Shuey DJ, "RNAi gene-silencing in therapeutic intervention" 7 : 1040-1046, 2002

      1 Hussain SP, "p53 mutation spectrum and load: the generation of hypotheses linking the exposure of endogenous or exogenous carcinogens to human carcinoma" 428 : 23-32, 1999

      2 Havre PA, "p53 inactivation by HPV16 E6 results in increased mutagenesis in human cells" 55 : 4420-4424, 1995

      3 Quintanilla-Martinez L, "p53 Mutations in nasal natural killer / T-cell lymphoma from Mexico:association with large cell morphology and advanced disease" 159 : 2095-2105, 2001

      4 Plasterk RH, "The silence of the genes" 10 : 562-567, 2000

      5 Schwarz E., "Stremalau A zur Hasusen H. Structure and transcription of human papilloma virus sequences in utrine cervix carcinoma cells" 314 : 111-114, 1985

      6 Gitlin L, "Short interfering RNA confers intracellular antiviral immunity in human cells" 418 : 430-434, 2002

      7 Matsukura T, "Relationships between 80 human papilloma virus genotypes and different grades of cervical intraepithelial neoplasia: association and causality" 283 (283): 39-47, 2001

      8 Hashiguchi Y, "Relationship between HPV typing and the status of G2 cell cycle regulators in cervical neoplasia" 12 : 587-591, 2004

      9 Taylor WR, "Regulation of the G2 / M transition by p53" 20 : 1803-1815, 2001

      10 Shuey DJ, "RNAi gene-silencing in therapeutic intervention" 7 : 1040-1046, 2002

      11 Ge Q, "RNA interference of influenza virus production by directly targeting mRNA for degradation and indirectly inhibiting all viral RNA transcription" 100 : 2718-2723, 2003

      12 Aoki Y, "RNA interference may be more potent than antisense RNA in human carcinoma cell lines" 30 : 96-102, 2003

      13 Cioca DP, "RNA interference is a functional pathway with therapeutic potential in human myeloid leukemia cell lines" 10 : 125-133, 2003

      14 McCaffrey AP, "RNA interference in adult mice" 418 (418): 38-39, 2002

      15 Tuschl T., "RNA interference and short interfering RNAs" 2 : 239-245, 2001

      16 Fire A, "Potent and specific genetic interference by double-stranded RNA in Caenorhabditis elegans" 391 : 806-811, 1998

      17 Cogoni C, "Post-transcriptional gene silencing across kingdoms" 10 : 638-643, 2000

      18 Wells SI, "Papilloma virus E2 induces senescence in HPVpositive cells via pRB- and p21(CIP)-dependent pathways" 19 : 5762-5771, 2000

      19 Bykov VJ, "Novel carcinoma therapy by reactivation of the p53 apoptosis pathway" 35 : 458-465, 2003

      20 Jacque JM, "Modulation of HIV-1replication by RNA interference" 418 : 435-438, 2002

      21 Lorincz AT, "Human papilloma virus infection of the cervix:relative risk associations of 15 common anogenital types" 79 : 328-337, 1992

      22 Munoz N, "Human papilloma virus and carcinoma: the epidemiological evidence" 19 : 1-5, 2003

      23 Gissman L, "Human papilloma virus (HPV): Characterization of 4 different isolates" 76 : 569-580, 1977

      24 Braun K, "HPV18 E6 and E7genes affect cell cycle, pRB and p53 of cervical tumor cells and represent prominent candidates for intervention by use peptide nucleic acids (PNAs)" 209 : 37-49, 2004

      25 Carmichael JW, "Evaluation of a tetrazolium-based semiautomated colorimetric assay: assessment of chemosensitivity testing" 47 : 936-942, 1987

      26 Tang D, "ERK activation mediates cell cycle arrest and apoptosis after DNA damage independently of p53" 277 : 12710-12717, 2002

      27 Bass BL, "Double-stranded RNA as a template for gene silencing" 101 : 235-238, 2000

      28 Bass BL., "Double-stranded RNA as a template for gene silencing" 01 : 235-238, 2000

      29 Kiyono T, "Binding of high-risk human papilloma virus E6 oncoproteins to the human homologue of the Drosophila discs large tumor suppressor protein" 94 : 11612-11616, 1997

      30 Hammond SM, "Argonaute 2, a link between genetic and biochemical analyses of RNAi" 293 : 1146-1150, 2002

      31 Ministry of Health and Welfare, "Annual Report of the Central Cancer Registry in Korea (2002. 1~2002. 12)" 2003

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2026 평가예정 재인증평가 신청대상 (재인증)
      2020-01-01 평가 등재학술지 유지 (재인증) KCI등재
      2017-01-01 평가 등재학술지 선정 (계속평가) KCI등재
      2016-01-01 평가 등재후보학술지 유지 (계속평가) KCI등재후보
      2015-01-08 학술지명변경 한글명 : 대한임상검사학회지 -> 대한임상검사과학회지
      외국어명 : 미등록 -> Korean Journal of Clinical Laboratory Science
      KCI등재후보
      2014-06-25 학회명변경 한글명 : 대한임상검사학회 -> 대한임상검사과학회
      영문명 : The Korean Society for Clinical Laboratory Science -> Korean Society for Clinical Laboratory Science
      KCI등재후보
      2014-01-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
      2004-12-17 학회명변경 영문명 : The Korean Society Of Biomedical Laboratory Science -> The Korean Society for Clinical Laboratory Science
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      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.43 0.43 0.36
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.31 0.28 0.34 0.12
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