Hypoxia-Inducible Factors as an Alternative Source of Treatment Strategy for Cancer

被引:74
作者
Akanji, Musbau Adewumi [1 ]
Rotimi, Damilare [2 ]
Adeyemi, Oluyomi Stephen [2 ]
机构
[1] Univ Ilorin, Dept Biochem, Ilorin, Nigeria
[2] Landmark Univ, Dept Biochem, Nanomed & Toxicol Lab, Med Biochem, Omu Aran 251101, Nigeria
关键词
TRANSCRIPTION FACTOR; MITOCHONDRIAL-DNA; HIF-ALPHA; D-LOOP; INHIBITION; PROTEIN; HIF-1-ALPHA; COMPLEX; VHL; METABOLISM;
D O I
10.1155/2019/8547846
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Hypoxia-inducible factors (HIFs) are transcription factors that activate the transcription of genes necessary to circumvent to hypoxic (low oxygen level) environments. In carcinogenesis, HIFs play a critical role. Indeed, HIF-1 alpha has been validated as a promising target for novel cancer therapeutics, even as clinical investigations have linked increased levels of HIF-1 alpha with aggressive cancer progression as well as poor patient prognosis. More so, inhibiting HIF-1 activity restricted cancer progression. Therefore, HIF-1 is a viable target for cancer therapy. This may be expected considering the fact that cancer cells are known to be hypoxic. In order to survive the hypoxic microenvironment, cancer cells activate several biochemical pathways via the HIF-1 alpha. Additionally, cellular and molecular insights have proved prospects of the HIF-1 alpha pathway for the development of novel anticancer treatment strategies. The biochemical importance of hypoxia-inducible factors (HIFs) cannot be overemphasized as carcinogenesis, cancer progression, and HIFs are intricately linked. Therefore, this review highlights the significance of these linkages and also the prospects of HIFs as an alternative source of cancer therapies.
引用
收藏
页数:10
相关论文
共 65 条
[1]
Adeyemi O.S., 2019, COMP CLIN PATHOL, V28, P949, DOI DOI 10.1007/s00580-018-2841-z
[2]
Single nucleotide polymorphisms in the D-loop region of mitochondrial DNA is associated with renal cell carcinoma outcome [J].
Bai, Yaling ;
Guo, Zhanjun ;
Xu, Jinsheng ;
Liu, Shufeng ;
Zhang, Junxia ;
Cui, Liwen ;
Zhang, Huiran ;
Zhang, Shenglei .
MITOCHONDRIAL DNA, 2015, 26 (02) :224-226
[3]
HIF-1 at the crossroads of hypoxia, inflammation, and cancer [J].
Balamurugan, Kuppusamy .
INTERNATIONAL JOURNAL OF CANCER, 2016, 138 (05) :1058-1066
[4]
Hypoxia-Induced Autophagy Is Mediated through Hypoxia-Inducible Factor Induction of BNIP3 and BNIP3L via Their BH3 Domains [J].
Bellot, Gregory ;
Garcia-Medina, Raquel ;
Gounon, Pierre ;
Chiche, Johanna ;
Roux, Daniele ;
Pouyssegur, Jacques ;
Mazure, Nathalie M. .
MOLECULAR AND CELLULAR BIOLOGY, 2009, 29 (10) :2570-2581
[5]
Stabilization of HIF-1α is critical to improve wound healing in diabetic mice [J].
Botusan, Ileana Ruxandra ;
Sunkari, Vivekananda Gupta ;
Savu, Octavian ;
Catrina, Anca Irinel ;
Grunler, Jacob ;
Lindberg, Stina ;
Pereira, Teresa ;
Yla-Herttuala, Seppo ;
Poellinger, Lorenz ;
Brismar, Kerstin ;
Catrina, Sergiu-Bogdan .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2008, 105 (49) :19426-19431
[6]
Mitochondrial mutations in cancer [J].
Brandon, M. ;
Baldi, P. ;
Wallace, D. C. .
ONCOGENE, 2006, 25 (34) :4647-4662
[7]
Hypoxia inducible factor (HIF) as a model for studying inhibition of protein-protein interactions [J].
Burslem, George M. ;
Kyle, Hannah F. ;
Nelson, Adam ;
Edwards, Thomas A. ;
Wilson, Andrew J. .
CHEMICAL SCIENCE, 2017, 8 (06) :4188-4202
[8]
Mitochondrial DNA mutations in human cancer [J].
Chatterjee, A. ;
Mambo, E. ;
Sidransky, D. .
ONCOGENE, 2006, 25 (34) :4663-4674
[9]
Synergistic Leukemia Eradication by Combined Treatment with Retinoic Acid and HIF Inhibition by EZN-2208 (PEG-SN38) in Preclinical Models of PML-RARα and PLZF-RARα-Driven Leukemia [J].
Coltella, Nadia ;
Valsecchi, Roberta ;
Ponente, Manfredi ;
Ponzoni, Maurilio ;
Bernardi, Rosa .
CLINICAL CANCER RESEARCH, 2015, 21 (16) :3685-3694
[10]
Loss of HIF-2 and inhibition of VEGF impair fetal lung maturation, whereas treatment with VEGF prevents fatal respiratory distress in premature mice [J].
Compernolle, V ;
Brusselmans, K ;
Acker, T ;
Hoet, P ;
Tjwa, M ;
Beck, H ;
Plaisance, S ;
Dor, Y ;
Keshet, E ;
Lupu, F ;
Nemery, B ;
Dewerchin, M ;
Van Veldhoven, P ;
Plate, K ;
Moons, L ;
Collen, D ;
Carmeliet, P .
NATURE MEDICINE, 2002, 8 (07) :702-710