c-Jun N-terminal Kinase (JNK), p38, and Caspases: Promising Therapeutic Targets for the Regulation of Apoptosis in Cancer Cells by Phytochemicals

被引:2
|
作者
Kumar, Manish [1 ]
Kaur, Satwinderjeet [2 ]
Kaur, Sandeep [2 ]
机构
[1] SD Coll, Barnala 148101, Punjab, India
[2] Guru Nanak Dev Univ, Dept Bot & Environm Sci, Amritsar 143005, Punjab, India
关键词
Cancer; apoptosis; caspases; chemoprevention; phytoconstituents; JNK pathway; ACTIVATED PROTEIN-KINASES; HUMAN PROSTATE-CANCER; CYCLE ARREST; SIGNAL-TRANSDUCTION; DOWN-REGULATION; LEAF EXTRACT; MITOCHONDRIAL DYSFUNCTION; INTRINSIC PATHWAY; AQUEOUS EXTRACT; GROWTH-FACTOR;
D O I
10.2174/1573394719666230817094831
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Carcinogenesis is a process in which uncontrolled cell proliferation forms preneoplastic nodules which precede the appearance of cancer. In normal cells, growth and proliferation are regulated by certain growth and hormonal stimulation, while mutational alterations in these signals render the cells independent and resistant to these signals. In cancer, the critical homeostatic balance between cell growth and apoptosis is lost and the cells continue to survive beyond their normal life span. The activation of c-Jun N-terminal kinase (JNK), p38 and caspases are involved in potential proapoptotic signaling pathways. JNK, p38 MAPK pathway and caspases play a crucial role in the control of apoptosis in response to stress. The most recent and up-to-date literature was evaluated in this study, which describes the role of JNK, p38 MAPK pathway and caspases as therapeutic target in cancer. Chemotherapy uses drugs that are cytotoxic to highly proliferating tumor cells but also kills the non-tumor rapidly proliferating cells in the hair, skin and gastrointestinal tract epithelium, thereby accounting the side effects of these types of treatments. Recently, chemopreventive modalities derived from phytoconstituents present in plants provide a broad-spectrum strategy to overcome the incidence of cancer. Non-toxic, safe and affordable bioavailabilities of chemopreventive agents provide credence support in the field of cancer research compared to conventional therapies that cause serious consequences. Chemoprevention envisages the basic mechanisms like modulating the activity of xenobiotic-metabolizing enzymes, induction of apoptosis, immune system activation, suppressing angiogenesis and the formation of metastasis, antioxidant and anti-inflammatory properties. The present review highlighted the role of phytoconstituents derived from food, vegetables and medicinal plants in the induction of apoptosis in cancer cells, which in turn is mediated by the activation of JNK, p38 MAPK pathways, and caspases.
引用
收藏
页码:200 / 211
页数:12
相关论文
共 50 条
  • [41] Activation of c-Jun N-Terminal Kinase (JNK) during Mitosis in Retinal Progenitor Cells
    Ribas, Vinicius Toledo
    Goncalves, Bruno Souza
    Linden, Rafael
    Chiarini, Luciana Barreto
    PLOS ONE, 2012, 7 (04):
  • [42] c-Jun N-terminal kinase (JNK) signaling: Recent advances and challenges
    Bogoyevitch, Marie A.
    Ngoei, Kevin R. W.
    Zhao, Teresa T.
    Yeap, Yvonne Y. C.
    Ng, Dominic C. H.
    BIOCHIMICA ET BIOPHYSICA ACTA-PROTEINS AND PROTEOMICS, 2010, 1804 (03): : 463 - 475
  • [43] Identification of c-Jun NH2-terminal protein kinase (JNK)-activating kinase 2 as an activator of JNK but not p38
    Lu, XH
    Nemoto, S
    Lin, AN
    JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (40) : 24751 - 24754
  • [44] Inhibition of the c-Jun N-terminal kinase (JNK) signaling pathway by curcumin
    Yi-Rong Chen
    Tse-Hua Tan
    Oncogene, 1998, 17 : 173 - 178
  • [45] Activaton of c-Jun N-terminal kinase (JNK) in experimental glaucoma in rats
    Kwong, JM
    Caprioli, J
    INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, 2004, 45 : U787 - U787
  • [46] Characterization of a novel JNK (c-Jun N-terminal kinase) inhibitory peptide
    Ngoei, Kevin R. W.
    Catimel, Bruno
    Church, Nicole
    Lio, Daisy S.
    Dogovski, Con
    Perugini, Matthew A.
    Watt, Paul M.
    Cheng, Heung-Chin
    Ng, Dominic C. H.
    Bogoyevitch, Marie A.
    BIOCHEMICAL JOURNAL, 2011, 434 : 399 - 413
  • [47] C-Jun N-Terminal Kinase 2 (JNK2) In Sepsis
    Sala, M.
    Gu, L.
    Walter, J. M.
    Chen, C.
    Do-Umehara, H.
    Zhang, Q.
    Reyfman, P. A.
    Anekalla, K.
    Budinger, G. S.
    Misharin, A. V.
    Wunderink, R. G.
    Liu, J.
    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2017, 195
  • [48] The role of c-jun N-terminal kinase (JNK) in Parkinson's disease
    Peng, J
    Andersen, JK
    IUBMB LIFE, 2003, 55 (4-5) : 267 - 271
  • [49] Inhibition of the c-Jun N-terminal kinase (JNK) signaling pathway by curcumin
    Chen, YR
    Tan, TH
    ONCOGENE, 1998, 17 (02) : 173 - 178
  • [50] Taxol-induced mitochondrial stress in melanoma cells is mediated by activation of c-Jun N-terminal kinase (JNK) and p38 pathways via uncoupling protein
    Selimovic, Denis
    Hassan, Mohamed
    Haikel, Youssef
    Hengge, Ulrich R.
    CELLULAR SIGNALLING, 2008, 20 (02) : 311 - 322