Targeting the Fas/FasL signaling pathway in cancer therapy

Villa‐Morales, María; Fernández‐Piqueras, José

doi:10.1517/14728222.2011.628937

Cited by 139 publications

(104 citation statements)

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“…In some instances cytokines and chemokines can recruit antitumor immune effector cells so as to control tumor progression (24,25); however, cytokines and chemokines in the tumor microenvironment usually recruit immunosuppressive cells to help tumor escape immunological attack and promote angiogenesis (20 -21, 26). Therefore, targeting Fas signaling or Fas signaling-initiated cancer-related inflammation may be helpful as a cancer therapeutic, which needs to be explored further (27). Cancer-related inflammation has many tumor-promoting effects, promoting cancer cell proliferation and survival, facilitating angiogenesis and cancer metastasis, and suppressing immune responses against cancer (28).…”

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confidence: 99%

Blockade of Fas Signaling in Breast Cancer Cells Suppresses Tumor Growth and Metastasis via Disruption of Fas Signaling-initiated Cancer-related Inflammation

Liu

Tan

Zheng

et al. 2014

Journal of Biological Chemistry

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Background:The non-apoptotic functions of Fas signaling have been proposed to play an important role in promoting tumor progression. Results: Blockade of Fas signaling suppresses tumor growth and metastasis via disruption of Fas signaling-initiated cancerrelated inflammation. Conclusion: Fas signaling-initiated cancer-related inflammation in breast cancer cells may be a potential target for cancer treatment.Significance: This study provides mechanistic insight into the role of Fas signaling in cancer-related inflammation.

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mentioning

confidence: 99%

Blockade of Fas Signaling in Breast Cancer Cells Suppresses Tumor Growth and Metastasis via Disruption of Fas Signaling-initiated Cancer-related Inflammation

Liu

Tan

Zheng

et al. 2014

Journal of Biological Chemistry

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“…The Fas gene is one of the most important regulatory genes for apoptosis, and the abnormalities in the Fas/FasL signaling pathway is associated with the occurrence and development of tumor and the sensitivity of tumor cells to certain chemotherapeutic reagents (18)(19)(20). However, the level of Fas gene expression is low in or even absent from certain ovarian cancer cells, which decreases the Fas-mediated apoptosis and chemosensitivity of these cells (1,12).…”

Section: Discussionmentioning

confidence: 99%

Therapeutic effect of targeted Fas-expressing adenoviruses method combining γδ T cells in a mouse model of human ovarian carcinoma

Zeng

Lin

et al. 2017

Oncol Lett

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Abstract. The present study aimed to investigate the therapeutic effect and safety of targeted use of Fas-expressing adenoviruses combined with γδ T cell-mediated killing to treat human ovarian cancer xenografts in BALB/c mice. Shuttle plasmids containing control elements of human telomerase reverse transcriptase promoter and two-step transcriptional amplification system were constructed and packaged into adenovirus-5 vectors to generate expression of an exogenous Fas gene. A mouse xenograft model of human ovarian carcinoma was constructed. A total of 35 BALB/c mice were randomly divided into five groups, which were injected with PBS, γδ T cells, Fas-expressing adenoviruses, taxol, or Fas-expressing adenovirus and γδ T cells. The weight and volume of tumors in mice in each group was monitored. Tissue sections of the various tissues of mice in the Fas-expressing adenovirus and γδ T cells group was compared with those in the PBS group to evaluate the safety of Fas-expressing adenovirus and γδ T cells in the treatment of human ovarian cancer xenograft tumors. The results of the present study indicated that mice in all treatment groups were alive at the end of the treatment course. Tumor weight and volume was the highest in the PBS group, followed successively by the adenovirus group, the γδ T cell group, the adenovirus and γδ T cell group, and the taxol group. The weight and volume inhibition rate in adenovirus and γδ T cell group were significantly higher compared with in the PBS group (P<0.05). Pathological observation of tissue samples revealed that none of vital organs in the adenovirus and γδ T cell group developed any evident morphological changes during treatment, when compared with healthy controls. In conclusion, the combined therapy with Fas-expressing adenoviruses and γδ T cells is efficient and safe for the treatment of mouse human ovarian carcinoma xenografts.

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“…The FAS gene, has a critical role in the tumor growth and metastasis (2). Two polymorphisms have been identified in the FAS promoter region one in the silencer region, G to A substitution at nucleotide position −670 (rs1800682) (3).…”

Section: Original Papermentioning

confidence: 99%

Strong Linkage Disequilibrium Between -670 A>G and -1377 G>A Polymorphisms in FAS Gene in Patients with Breast Cancer and Controls

Ghochan¹,

Mohammadi²,

Jalali³

et al. 2016

The Cancer Press

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Original PaperBreast cancer is developed from the breast tumors.There are more than 18 sub-types of this cancer. This type of cancer is the second cause of mortality in women (1,2). The etiology of breast cancer is multi factorial. Genetic factors are interfered in the etiology of breast cancer. The FAS gene, has a critical role in the tumor growth and metastasis (2). Two polymorphisms have been identified in the FAS promoter region one in the silencer region, G to A substitution at nucleotide position −670 (rs1800682) (3).Breast cancer is the second cause of mortality in women. The etiology of breast cancer is multi factorial. Genetic factors play an important role in the etimology of breast cancer. The FAS gene, has a critical role in the tumor growth and metastasis. Gene polymorphisms including -1377 G>A and -670 A/G in FAS gene have shown to change the transcription activities of this gene. The FAS genotypes were determined by polymerase chain reactionrestriction fragment length polymorphism (PCR-RFLP) in 115 breast cancer patients, 115 healthy controls, all female and selected from city of Mashhad in north-eastern part of Iran. BstuI and ScrfI were used as endonuclease enzymes to detect -1377G/A and -670A/G gene polymorphisms, respectively. GG, GA and AA genotype frequencies for FAS -1377 polymorphism in patients were 30.4%, 49.6% and 20%, whereas in healthy controls were 26.1%, 50.4% and 23.5%, respectively and there was no significant difference between case and controls (p=0.7).Additionally, genotype frequencies of FAS -670 AA, AG and GG in patient groups were 52.2%, 39.1% and 8.7% respectively . The result of genotype frequency in controls for FAS -670 AA, AG and GG was 47%, 41% and 10.4%, which Showed insignificant difference as compared with patients genotypes (p=0.78). These results showed that FAS−1377G/A and FAS -670 A/G gene polymorphisms had a strong linkage disequilibrium with p value <0.001. These results indicated the lack of association between FAS−1377G>A and FAS -670 A/G gene polymorphisms and risk of breast cancer. Moreover, a significant linkage disequilibrium was found betweenFAS−1377G/A and FAS -670 A/G gene polymorphisms in case and control groups.

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Targeting the Fas/FasL signaling pathway in cancer therapy

Abstract: The success of the Fas/FasL system targeting for therapeutics will require a better understanding of the alterations conferring resistance, in order to use the most appropriate sensitizing chemotherapeutic or radiotherapeutic agents in combination with effective targeted therapies.

Cited by 139 publications

References 144 publications

Blockade of Fas Signaling in Breast Cancer Cells Suppresses Tumor Growth and Metastasis via Disruption of Fas Signaling-initiated Cancer-related Inflammation

Blockade of Fas Signaling in Breast Cancer Cells Suppresses Tumor Growth and Metastasis via Disruption of Fas Signaling-initiated Cancer-related Inflammation

Therapeutic effect of targeted Fas-expressing adenoviruses method combining γδ T cells in a mouse model of human ovarian carcinoma

Strong Linkage Disequilibrium Between -670 A>G and -1377 G>A Polymorphisms in FAS Gene in Patients with Breast Cancer and Controls

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