RISS 학술연구정보서비스

검색
다국어 입력

http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.

변환된 중국어를 복사하여 사용하시면 됩니다.

예시)
  • 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
  • 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
닫기
    인기검색어 순위 펼치기

    RISS 인기검색어

      KCI등재 SCOPUS SCIE

      Knockdown of Pyruvate Kinase M Inhibits Cell Growth and Migration by Reducing NF-kB Activity in Triple-Negative Breast Cancer Cells

      한글로보기

      https://www.riss.kr/link?id=A106373043

      • 0

        상세조회
      • 0

        다운로드
      서지정보 열기
      • 내보내기
      • 내책장담기
      • 공유하기
      • 오류접수

      부가정보

      다국어 초록 (Multilingual Abstract)

      Altered genetic features in cancer cells lead to a high rate of aerobic glycolysis and metabolic reprogramming that is essential for increased cancer cell viability and rapid proliferation. Pyruvate kinase muscle (PKM) is a rate-limiting enzyme in the...

      Altered genetic features in cancer cells lead to a high rate of aerobic glycolysis and metabolic reprogramming that is essential for increased cancer cell viability and rapid proliferation. Pyruvate kinase muscle (PKM) is a rate-limiting enzyme in the final step of glycolysis. Herein, we report that PKM is a potential therapeutic target in triple-negative breast cancer (TNBC) cells. We found that PKM1 or PKM2 is highly expressed in TNBC tissues or cells. Knockdown of PKM significantly suppressed cell proliferation and migration, and strongly reduced S phase and induced G2 phase cell cycle arrest by reducing phosphorylation of the CDC2 protein in TNBC cells. Additionally, knockdown of PKM significantly suppressed NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) activity by reducing the phosphorylation of p65 at serine 536, and also decreased the expression of NF-kB target genes. Taken together, PKM is a potential target that may have therapeutic implications for TNBC cells.

      더보기

      참고문헌 (Reference)

      1 Vander Heiden, M. G., "Understanding the Warburg effect : the metabolic requirements of cell proliferation" 324 : 1029-1033, 2009

      2 Kroemer, G., "Tumor cell metabolism : cancer's Achilles' heel" 13 : 472-482, 2008

      3 Ito-Kureha, T., "Tropomodulin 1 expression driven by NF-kappaB enhances breast cancer growth" 75 : 62-72, 2015

      4 Bianchini, G., "Triple-negative breast cancer : challenges and opportunities of a heterogeneous disease" 13 : 674-690, 2016

      5 Okazaki, M., "The effect of HIF-1alpha and PKM1 expression on acquisition of chemoresistance" 10 : 1865-1874, 2018

      6 DeBerardinis, R. J., "The biology of cancer : metabolic reprogramming fuels cell growth and proliferation" 7 : 11-20, 2008

      7 Christofk, H. R., "The M2 splice isoform of pyruvate kinase is important for cancer metabolism and tumour growth" 452 : 230-233, 2008

      8 Israel, A., "The IKK complex, a central regulator of NF-kappaB activation" 2 : a000158-, 2010

      9 Tennant, D. A., "Targeting metabolic transformation for cancer therapy" 10 : 267-277, 2010

      10 Barbie, T. U., "Targeting an IKBKE cytokine network impairs triple-negative breast cancer growth" 124 : 5411-5423, 2014

      1 Vander Heiden, M. G., "Understanding the Warburg effect : the metabolic requirements of cell proliferation" 324 : 1029-1033, 2009

      2 Kroemer, G., "Tumor cell metabolism : cancer's Achilles' heel" 13 : 472-482, 2008

      3 Ito-Kureha, T., "Tropomodulin 1 expression driven by NF-kappaB enhances breast cancer growth" 75 : 62-72, 2015

      4 Bianchini, G., "Triple-negative breast cancer : challenges and opportunities of a heterogeneous disease" 13 : 674-690, 2016

      5 Okazaki, M., "The effect of HIF-1alpha and PKM1 expression on acquisition of chemoresistance" 10 : 1865-1874, 2018

      6 DeBerardinis, R. J., "The biology of cancer : metabolic reprogramming fuels cell growth and proliferation" 7 : 11-20, 2008

      7 Christofk, H. R., "The M2 splice isoform of pyruvate kinase is important for cancer metabolism and tumour growth" 452 : 230-233, 2008

      8 Israel, A., "The IKK complex, a central regulator of NF-kappaB activation" 2 : a000158-, 2010

      9 Tennant, D. A., "Targeting metabolic transformation for cancer therapy" 10 : 267-277, 2010

      10 Barbie, T. U., "Targeting an IKBKE cytokine network impairs triple-negative breast cancer growth" 124 : 5411-5423, 2014

      11 Hayden, M. S., "Shared principles in NF-kappaB signaling" 132 : 344-362, 2008

      12 Kuo, W. Y., "STAT3/NF-kappaB-regulated lentiviral TK/GCV suicide gene therapy for Cisplatin-resistant triple-negative breast cancer" 7 : 647-663, 2017

      13 Chaneton, B., "Rocking cell metabolism : revised functions of the key glycolytic regulator PKM2 in cancer" 37 : 309-316, 2012

      14 Mazurek, S., "Pyruvate kinase type M2: a key regulator within the tumour metabolome and a tool for metabolic profiling of tumours" (4) : 99-124, 2007

      15 Mazurek, S., "Pyruvate kinase type M2 : a key regulator of the metabolic budget system in tumor cells" 43 : 969-980, 2011

      16 Kim, D. J., "Pyruvate kinase isoenzyme M2 is a therapeutic target of gemcitabine-resistant pancreatic cancer cells" 336 : 119-129, 2015

      17 Chiavarina, B., "Pyruvate kinase expression(PKM1 and PKM2)in cancer-associated fibroblasts drives stromal nutrient production and tumor growth" 12 : 1101-1113, 2011

      18 Gao, X., "Pyruvate kinase M2regulates gene transcription by acting as a protein kinase" 45 : 598-609, 2012

      19 Luo, W., "Pyruvate kinase M2 regulates glucose metabolism by functioning as a coactivator for hypoxia-inducible factor 1in cancer cells" 2 : 551-556, 2011

      20 Luo, W., "Pyruvate kinase M2 is a PHD3-stimulated coactivator for hypoxia-inducible factor 1" 145 : 732-744, 2011

      21 Nabel, G. J., "Proposed NF-kappa B/I kappa B family nomenclature" 7 : 2063-, 1993

      22 Chang, B., "Prolonged progression-free survival in a patient with triple-negative breast cancer metastatic to the liver after chemotherapy and local radiation therapy" 14 : e61-e64, 2014

      23 Azoitei, N., "PKM2 promotes tumor angiogenesis by regulating HIF-1alpha through NF-kappaB activation" 15 : 3-, 2016

      24 Yang, W., "PKM2 phosphorylates histone H3and promotes gene transcription and tumorigenesis" 150 : 685-696, 2012

      25 Harris, I., "PKM2 : a gatekeeper between growth and survival" 22 : 447-449, 2012

      26 Morita, M., "PKM1 confers metabolic advantages and promotes cell-autonomous tumor cell growth" 33 : 355.e7-367.e7, 2018

      27 Zhou, Z., "Oncogenic kinase-induced PKM2 tyrosine 105phosphorylation converts nononcogenic PKM2 to a tumor promoter and induces cancer stem-like cells" 78 : 2248-2261, 2018

      28 Han, D., "NF-kappaB/RelA-PKM2 mediates inhibition of glycolysis by fenofibrate in glioblastoma cells" 6 : 26119-26128, 2015

      29 Tennant, D. A., "Metabolic transformation in cancer" 30 : 1269-1280, 2009

      30 Bonotto, M., "Measures of outcome in metastatic breast cancer : insights from a real-world scenario" 19 : 608-615, 2014

      31 Dang, C. V., "Links between metabolism and cancer" 26 : 877-890, 2012

      32 Wang, H. J., "JMJD5 regulates PKM2 nuclear translocation and reprograms HIF-1alpha-mediated glucose metabolism" 111 : 279-284, 2014

      33 House, C. D., "IΚΚε cooperates with either MEK or non-canonical NF-kB driving growth of triple-negative breast cancer cells in different contexts" 18 : 595-, 2018

      34 Anastasiou, D., "Inhibition of pyruvate kinase M2 by reactive oxygen species contributes to cellular antioxidant responses" 334 : 1278-1283, 2011

      35 King, A., "Glucose metabolism and programmed cell death : an evolutionary and mechanistic perspective" 21 : 885-893, 2009

      36 Wu, X., "Global phosphotyrosine survey in triple-negative breast cancer reveals activation of multiple tyrosine kinase signaling pathways" 6 : 29143-29160, 2015

      37 Yang, W., "ERK1/2-dependent phosphorylation and nuclear translocation of PKM2 promotes the Warburg effect" 14 : 1295-1304, 2012

      38 Yamaguchi, N., "Constitutive activation of nuclear factor-kappaB is preferentially involved in the proliferation of basal-like subtype breast cancer cell lines" 100 : 1668-1674, 2009

      39 Tutt, A., "Carboplatin in BRCA1/2-mutated and triple-negative breast cancer BRCAness subgroups : the TNT Trial" 24 : 628-637, 2018

      40 Fantin, V. R., "Attenuation of LDH-A expression uncovers a link between glycolysis, mitochondrial physiology, and tumor maintenance" 9 : 425-434, 2006

      41 Lebert, J. M., "Advances in the systemic treatment of triple-negative breast cancer" 25 (25): S142-S150, 2018

      42 Lv, L., "Acetylation targets the M2 isoform of pyruvate kinase for degradation through chaperone-mediated autophagy and promotes tumor growth" 42 : 719-730, 2011

      43 Qiao, Y., "AP-1 is a key regulator of Proinflammatory cytokine TNFalphamediated triple-negative breast cancer progression" 291 : 5068-5079, 2016

      더보기

      동일학술지(권/호) 다른 논문

      동일학술지 더보기

      더보기

      분석정보

      View

      상세정보조회

      0

      Usage

      원문다운로드

      0

      대출신청

      0

      복사신청

      0

      EDDS신청

      0

      동일 주제 내 활용도 TOP

      더보기

      주제

      연도별 연구동향

      연도별 활용동향

      연관논문

      연구자 네트워크맵

      공동연구자 (7)

      유사연구자 (20) 활용도상위20명

      인용정보 인용지수 설명보기

      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
      2012-11-07 학술지명변경 한글명 : 분자와 세포 -> Molecules and Cells KCI등재
      2008-01-01 평가 SCI 등재 (등재유지) KCI등재
      2006-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2004-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2001-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      1998-07-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
      더보기

      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 2.77 0.19 1.85
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      1.37 1.11 0.379 0.03
      더보기

      이 자료와 함께 이용한 RISS 자료

      나만을 위한 추천자료

      해외이동버튼