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      KCI등재 SCOPUS SCIE

      KAT5 Negatively regulates the proliferation of prostate cancer LNCaP cells via the caspase 3-dependent apoptosis pathway

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      https://www.riss.kr/link?id=A106333165

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      다국어 초록 (Multilingual Abstract) kakao i 다국어 번역

      Prostate cancer is one of the most common cancers in men over the age of sixty. Lysine acetyltransferase 5 (KAT5) is a histone acetyltransferase involved in transcriptional regulation, DNA repair, and cell signaling pathways. Previous studies have shown that KAT5 expression is reduced in the cytoplasm of the prostate cancer cell line LNCaP when exposed to androgen. Moreover, KAT5 has been reported to have a role in the molecular pathway leading to androgen-independent prostate cancer after long-term androgen deprivation therapy. Here, we showed that KAT5 expression was significantly reduced in prostate cancer tissues and cell lines by using the public databases Oncomine and Human Protein Atlas. Reduced KAT5 expression was significantly associated with high mortality in prostate cancer patients. Furthermore, KAT5 overexpression increased the level of apoptotic markers, such as cleaved-caspase 3, in LNCaP cells, thus enhancing the apoptotic death of LNCaP cells. Taken together, KAT5 induced apoptosis in prostate cancer cells via the caspase-3 pathway, indicating that KAT5 could be a gene therapy target for prostate cancer.
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      Prostate cancer is one of the most common cancers in men over the age of sixty. Lysine acetyltransferase 5 (KAT5) is a histone acetyltransferase involved in transcriptional regulation, DNA repair, and cell signaling pathways. Previous studies have sho...

      Prostate cancer is one of the most common cancers in men over the age of sixty. Lysine acetyltransferase 5 (KAT5) is a histone acetyltransferase involved in transcriptional regulation, DNA repair, and cell signaling pathways. Previous studies have shown that KAT5 expression is reduced in the cytoplasm of the prostate cancer cell line LNCaP when exposed to androgen. Moreover, KAT5 has been reported to have a role in the molecular pathway leading to androgen-independent prostate cancer after long-term androgen deprivation therapy. Here, we showed that KAT5 expression was significantly reduced in prostate cancer tissues and cell lines by using the public databases Oncomine and Human Protein Atlas. Reduced KAT5 expression was significantly associated with high mortality in prostate cancer patients. Furthermore, KAT5 overexpression increased the level of apoptotic markers, such as cleaved-caspase 3, in LNCaP cells, thus enhancing the apoptotic death of LNCaP cells. Taken together, KAT5 induced apoptosis in prostate cancer cells via the caspase-3 pathway, indicating that KAT5 could be a gene therapy target for prostate cancer.

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      참고문헌 (Reference)

      1 Halkidou K, "Upregulation and nuclear recruitment of HDAC1 in hormone refractory prostate cancer" 59 : 177-189, 2004

      2 Tang Y, "Tip60-dependent acetylation of p53 modulates the decision between cell-cycle arrest and apoptosis" 24 : 827-839, 2006

      3 Furdas SD, "Small molecule inhibitors of histone acetyltransferases as epigenetic tools and drug candidates" 345 : 7-21, 2012

      4 Dai Y, "Sirtuin 1 is required for antagonist-induced transcriptional repression of androgen-responsive genes by the androgen receptor" 21 : 1807-1821, 2007

      5 McGuire A, "Quantifying Tip60(Kat5)stratifies breast cancer" 9-, 2019

      6 Ortega-Atienza S, "Proteasome activity is important for replication recovery, CHK1 phosphorylation and prevention of G2 arrest after low-dose formaldehyde" 286 : 135-141, 2015

      7 Korkmaz CG, "Potentiation of androgen receptor transcriptional activity by inhibition of histone deacetylation-rescue of transcriptionally compromised mutants" 182 : 377-389, 2004

      8 van der Steen T, "Posttranslational Modification of the Androgen Receptor in Prostate Cancer" 14 : 14833-14859, 2013

      9 Munster PN, "Phase I trial of vorinostat and doxorubicin in solid tumours : histone deacetylase 2 expression as a predictive marker" 101 : 1044-1050, 2009

      10 Fu MF, "P300and p300/cAMP-response element-binding protein-associated factor acetylate the androgen receptor at sites governing hormone-dependent transactivation" 275 : 20853-20860, 2000

      1 Halkidou K, "Upregulation and nuclear recruitment of HDAC1 in hormone refractory prostate cancer" 59 : 177-189, 2004

      2 Tang Y, "Tip60-dependent acetylation of p53 modulates the decision between cell-cycle arrest and apoptosis" 24 : 827-839, 2006

      3 Furdas SD, "Small molecule inhibitors of histone acetyltransferases as epigenetic tools and drug candidates" 345 : 7-21, 2012

      4 Dai Y, "Sirtuin 1 is required for antagonist-induced transcriptional repression of androgen-responsive genes by the androgen receptor" 21 : 1807-1821, 2007

      5 McGuire A, "Quantifying Tip60(Kat5)stratifies breast cancer" 9-, 2019

      6 Ortega-Atienza S, "Proteasome activity is important for replication recovery, CHK1 phosphorylation and prevention of G2 arrest after low-dose formaldehyde" 286 : 135-141, 2015

      7 Korkmaz CG, "Potentiation of androgen receptor transcriptional activity by inhibition of histone deacetylation-rescue of transcriptionally compromised mutants" 182 : 377-389, 2004

      8 van der Steen T, "Posttranslational Modification of the Androgen Receptor in Prostate Cancer" 14 : 14833-14859, 2013

      9 Munster PN, "Phase I trial of vorinostat and doxorubicin in solid tumours : histone deacetylase 2 expression as a predictive marker" 101 : 1044-1050, 2009

      10 Fu MF, "P300and p300/cAMP-response element-binding protein-associated factor acetylate the androgen receptor at sites governing hormone-dependent transactivation" 275 : 20853-20860, 2000

      11 Farria A, "KATs in cancer : functions and therapies" 34 : 4901-4913, 2015

      12 Cregan S, "KAT5(Tip60)is a potential therapeutic target in malignant pleural mesothelioma" 48 : 1290-1296, 2016

      13 He W, "KAT5 and KAT6B are in positive regulation on cell proliferation of prostate cancer through PI3K-AKT signaling" 6 : 2864-2871, 2013

      14 Gregoire JM, "Identification of epigenetic factors regulating the mesenchyme to epithelium transition by RNA interference screening in breast cancer cells" 16 : 700-, 2016

      15 Kamine J, "Identification of a cellular protein that specifically interacts with the essential cysteine region of the HIV-1 tat transactivator" 216 : 357-366, 1996

      16 Weichert W, "Histone deacetylases 1, 2 and 3 are highly expressed in prostate cancer and HDAC2 expression is associated with shorter PSA relapse time after radical prostatectomy" 98 : 604-610, 2008

      17 Seligson DB, "Global histone modification patterns predict risk of prostate cancer recurrence" 435 : 1262-1266, 2005

      18 Halkidou K, "Expression of Tip60, an androgen receptor coactivator, and its role in prostate cancer development" 22 : 2466-2477, 2003

      19 Berns K, "A large-scale RNAi screen in human cells identifies new components of the p53 pathway" 428 : 431-437, 2004

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2023 평가예정 해외DB학술지평가 신청대상 (해외등재 학술지 평가)
      2020-01-01 평가 등재학술지 유지 (해외등재 학술지 평가) KCI등재
      2010-02-02 학회명변경 한글명 : 한국동물학회 -> 한국통합생물학회
      영문명 : 미등록 -> The Korean Society for Integrative Biology
      KCI등재
      2010-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2008-02-26 학술지명변경 한글명 : Integrative Biosciences -> Animal Cells and Systems
      외국어명 : Integrative Biosciences -> Animal Cells and Systems
      KCI등재
      2008-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2006-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2005-04-15 학술지등록 한글명 : Integrative Biosciences
      외국어명 : Integrative Biosciences
      KCI등재
      2004-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2001-07-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      1999-01-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.45 0.24 0.33
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.28 0.26 0.395 0.04
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