HIF-1α-dependent autophagy protects HeLa cells from fenretinide (4-HPR)-induced apoptosis in hypoxia☆

Liu, Xiao Wen; Su, Yi; Zhu, Hong; Cao, Ji; Ding, Wan Jing; Zhao, Yu; He, Qiao; Yang, Bo

doi:10.1016/j.phrs.2010.07.002

Cited by 75 publications

(59 citation statements)

References 49 publications

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“…Many of these HIF-1 inducible genes such as VEGF, Glut-1, MDR, and Bcl-2 directly or indirectly mediate chemoresistance 19 .Therefore, in a wide range of different tumor types, e.g. hepatocellular carcinoma, neuroblastoma, and lung cancer, inhibition of HIF-1α resensitizes cells to drug treatment in hypoxia and is then a valid target to reverse hypoxia-induced drug resistance 8,9,15,19,21,25,[27][28][29][30]56 . HIF-1α accumulation has been associated with shorter survival in patients with early stage cervical, breast, ovarian, endometrial, oropharyngeal squamous cell carcinoma, and oligodendroglioma.…”

Section: Hif-1 and Chemoresistancementioning

confidence: 99%

“…In this context, the most studied transcription factor is hypoxia-inducible factor-1 (HIF-1). HIF-1 is an important factor in the adaptation of cells to hypoxic environments, and significantly contributes to the aggressiveness and chemoresistance of number of different tumours 5,[7][8][9]15,19,21,[25][26][27][28][29][30] . However, these changes can be independent of HIF-1 (ref.…”

Section: Introduction -Hypoxia-induced Chemoresistancementioning

confidence: 99%

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Hypoxia-induced chemoresistance in cancer cells: The role of not only HIF-1

et al. 2015

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Background. The aim of this review is to provide the information about molecular basis of hypoxia-induced chemoresistance, focusing on the possibility of diagnostic and therapeutic use. Results. Hypoxia is a common feature of tumors and represents an independent prognostic factor in many cancers. It is the result of imbalances in the intake and consumption of oxygen caused by abnormal vessels in the tumor and the rapid proliferation of cancer cells. Hypoxia-induced resistance to cisplatin, doxorubicin, etoposide, melphalan, 5-flouoruracil, gemcitabine, and docetaxel has been reported in a number of experiments. Adaptation of tumor cells to hypoxia has important biological effects. The most studied factor responsible for these effects is hypoxia-inducible factor-1 (HIF-1) that significantly contributes to the aggressiveness and chemoresistance of different tumors. The HIF-1 complex, induced by hypoxia, binds to target genes, thereby increasing the expression of many genes. In addition, the expression of hundreds of genes can be also decreased in response to hypoxia in HIF-1 dependent manner, but without the detection of HIF-1 in these genes' promoters. HIF-1 independent mechanisms for drug resistance in hypoxia have been described, however, they are still rarely reported. The first clinical studies focusing on diagnosis of hypoxia and on inhibition of hypoxia-induced changes in cancer cells are starting to yield results. Conclusions. The adaptation to hypoxia requires many genetic and biochemical responses that regulate one another. Hypoxia-induced resistance is a very complex field and we still know very little about it. Different approaches to circumvent hypoxia in tumors are under development.

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Section: Hif-1 and Chemoresistancementioning

confidence: 99%

Section: Introduction -Hypoxia-induced Chemoresistancementioning

confidence: 99%

Hypoxia-induced chemoresistance in cancer cells: The role of not only HIF-1

et al. 2015

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“…Proteins were fractionated on 8% to 15% Tris-glycine gels, and then were transferred to PVDF membrane (Millipore, Bedford, MA, USA) and probed with primary antibodies (dilution range 1:500-1:1000) followed by horseradish peroxidase-labeled secondary antibodies at a 1:5000 dilution. Antibody binding was then detected using a chemiluminescent substrate and visualized on autoradiography film [17] .…”

Section: Cell Lysate Preparation and Western Blot Analysismentioning

confidence: 99%

In vitro anti-cancer activity of chamaejasmenin B and neochamaejasmin C isolated from the root of Stellera chamaejasme L

et al. 2012

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Aim: To examine the anti-cancer effects of chamaejasmenin B and neochamaejasmin C, two biflavonones isolated from the root of Stellera chamaejasme L (known as the traditional Chinese herb Rui Xiang Lang Du) in vitro. Methods: Human liver carcinoma cell lines (HepG2 and SMMC-7721), a human non-small cell lung cancer cell line (A549), human osteosarcoma cell lines (MG63, U2OS, and KHOS), a human colon cancer cell line (HCT-116) and a human cervical cancer cell line (HeLa) were used. The anti-proliferative effects of the compounds were measured using SRB cytotoxicity assay. DNA damage was detected by immunofluorescence and Western blotting. Apoptosis and cell cycle distribution were assessed using flow cytometry analysis. The expression of the related proteins was examined with Western blotting analysis. Results: Both chamaejasmenin B and neochamaejasmin C exerted potent anti-proliferative effects in the 8 human solid tumor cell lines. Chamaejasmenin B (the IC 50 values ranged from 1.08 to 10.8 μmol/L) was slightly more potent than neochamaejasmin C (the IC 50 values ranged from 3.07 to 15.97 μmol/L). In the most sensitive A549 and KHOS cells, the mechanisms underlying the anti-proliferative effects were characterized. The two compounds induced prominent expression of the DNA damage marker γ-H2AX as well as apoptosis. Furthermore, treatment of the cells with the two compounds caused prominent G 0 /G 1 phase arrest. Conclusion: Chamaejasmenin B and neochamaejasmin C are potential anti-proliferative agents in 8 human solid tumor cell lines in vitro via inducing cell cycle arrest, apoptosis and DNA damage.

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“…In this regard, it has been observed that hypoxia-mediated failure of cytotoxic treatment in vitro can be conferred via HIF1α-dependent induction of autophagy [75]. This process is mediated by the atypical BH3-only proteins such as the Bcl-2/E1B 19 kDa-interacting protein 3 (BNIP3/BNIP3L (NIX)) that are induced by HIF1α [74].…”

Section: Hifs and Cell Death Pathways: Apoptosis And Autophagymentioning

confidence: 99%

The Role of Hypoxia-Inducible Factors in Cancer Resistance

Saint-Martin¹,

Castañeda-Patlán²,

Robles-Flores³

2017

J Cell Signal

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Diminished oxygen availability (hypoxia) is a hallmark of the tumor microenvironment. A major regulator of cellular adaptation to hypoxia is the hypoxia-inducible factor (HIF) family of transcription factors, which play key roles in many crucial aspects of cancer biology including angiogenesis, stem cell maintenance, metabolic reprogramming, resistance to apoptosis, autocrine growth factor signaling, the EMT program, invasion and metastasis.Resistance to chemotherapy/radiotherapy is the primary cause for treatment failure in clinical oncology. Hypoxia and accumulation of hypoxia-inducible factors (HIFs) in solid tumors have been associated with resistance to treatment and poor prognosis. HIFs causes autophagy establishment to promote survival of cancer cells, and is also associated with the promotion and maintenance of cancer stem cells, a minority subpopulation within the tumor responsible for tumor recurrence and resistance to chemotherapy.In this review, we provide a concise comparative description of the structure, regulation, transcribed genes and roles played by each HIFα subunit in coordinating the transcriptional responses to hypoxia and on the roles they play in the promotion of resistance to anti-cancer therapy.

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HIF-1α-dependent autophagy protects HeLa cells from fenretinide (4-HPR)-induced apoptosis in hypoxia☆

Cited by 75 publications

References 49 publications

Hypoxia-induced chemoresistance in cancer cells: The role of not only HIF-1

Hypoxia-induced chemoresistance in cancer cells: The role of not only HIF-1

In vitro anti-cancer activity of chamaejasmenin B and neochamaejasmin C isolated from the root of Stellera chamaejasme L

The Role of Hypoxia-Inducible Factors in Cancer Resistance

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