Apoptosis induction by dohevanil, a DHA substitutive analog of capsaicin, in MCF-7 cells

Tuoya,; Baba, Naomichi; Shimoishi, Yasuaki; Murata, Yoshiyuki; Tada, Mikiro; Koseki, Masamichi; Takahata, Kyoya

doi:10.1016/j.lfs.2005.07.019

Cited by 31 publications

(31 citation statements)

References 16 publications

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“…In contrast, capsaicin treatment led to a decrease in the ROS level of MCF-7 cells. These results were inconsistent with what has been observed in H-ras-transformed MCF10A cells, in which the generation of ROS was believed to be essential for the inhibitory effect of capsaicin on cell growth, possibly by suppressing Rac 1 activity (18,25,26).…”

Section: Discussioncontrasting

confidence: 70%

“…In normal cells, however, capsaicin is largely ineffective. (18) Tuoya et al demonstrated that capsaicin induced apoptosis in human breast cancer MCF-7 cells (18) via a caspase-dependent pathway not involving caspase-3. Nevertheless, there is no study on the relationship between the caspase-independent pathway and capsaicin-induced apoptosis in human breast cancer cells at present.…”

Section: Introductionmentioning

confidence: 99%

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Capsaicin-induced apoptosis in human breast cancer MCF-7 cells through caspase-independent pathway

Chen¹

2009

Oncol Rep

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Abstract. , a significant pungent ingredient in a variety of red peppers of the genus Capsicum, is a type of vanilloid. It has been shown to exert biological activities (anticarcinogenic, antimutagenic and chemopreventive) in many cancer cell lines. It was found that capsaicin induces dose-dependent growth inhibition of MCF-7 cells, which does not express caspase-3. In this study, we investigated the molecular mechanism of capsaicin-induced apoptosis in MCF-7 cells. Treatment with capsaicin for 24 h resulted in dose-dependent apoptosis in these cells. After the addition of capsaicin, the levels of reactive oxygen species were reduced slightly in the earlier stage of treatment. Interestingly, an elevation of intracellular calcium ion concentration was detected in the MCF-7 cells. In time course and dosage studies, the mitochondrial membrane potential of MCF-7 cells decreased. However, the change was not significant. It is worth noting that the apoptosis-inducing factor translocated into the cytosol and nucleus from the mitochondria. Our results suggest that capsaicin induces cellular apoptosis through a caspase-independent pathway in MCF-7 cells, and that reactive oxygen species and intracellular calcium ion fluctuation has a minimal role in the process.

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Section: Discussioncontrasting

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Capsaicin-induced apoptosis in human breast cancer MCF-7 cells through caspase-independent pathway

Chen¹

2009

Oncol Rep

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“…This alkaloid compound has an in vitro antiproliferative effect on prostate (Mori et al, 2006;Sa´nchez et al, 2006), colon (Kim et al, 2004), gastric (Lo et al, 2005), hepatic (Jung et al, 2001) and leukemic cancer cells (Ito et al, 2004) while leaving normal cells unharmed (Ito et al, 2004;Athanasiou et al, 2007). One study so far showed growth-inhibitory effects of capsaicin on single MCF-7 breast cancer cell line but gave no detailed insights into the potential underlying molecular mechanisms (Tuoya et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Capsaicin causes cell-cycle arrest and apoptosis in ER-positive and -negative breast cancer cells by modulating the EGFR/HER-2 pathway

et al. 2009

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Capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide) is an ingredient of chili peppers with inhibitory effects against cancer cells of different origin. We examined the activity of capsaicin on breast cancer cells in vitro and in vivo. The drug potently inhibited growth of ER-positive (MCF-7, T47D, BT-474) and ER-negative (SKBR-3, MDA-MB231) breast cancer cell lines, which was associated with G 0 /G 1 cell-cycle arrest, increased levels of apoptosis and reduced protein expression of human epidermal growth factor receptor (EGFR), HER-2, activated extracellular-regulated kinase (ERK) and cyclin D1. In contrast, cell-cycle regulator p27 KIP1, caspase activity as well as poly-ADP ribose polymerase (PARP) cleavage were increased. Notably, capsaicin blocked breast cancer cell migration in vitro and decreased by 50% the size of MDA-MB231 breast cancer tumors growing orthotopically in immunodeficient mice without noticeable drug side effects. in vivo activation of ERK was clearly decreased, as well as expression of HER-2 and cyclin D1, whereas caspase activity and PARP cleavage products were increased in tumors of drug-treated mice. Besides, capsaicin potently inhibited the development of preneoplastic breast lesions by up to 80% without evidence of toxicity. Our data indicate that capsaicin is a novel modulator of the EGFR/HER-2 pathway in both ERpositive and -negative breast cancer cells with a potential role in the treatment and prevention of human breast cancer.

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“…It induced apoptosis of glioma cells, 5 hepatocellular carcinoma cells, 6 human esophagus epidermoid cells, 7 human leukemia cells 8 and human breast cancer cells. 9 Activation of caspase-3 was involved in capsaicin-induced cell death. [7][8][9] In vivo experiments support the results seen in cell lines.…”

Section: Discussionmentioning

confidence: 99%

“…9 Activation of caspase-3 was involved in capsaicin-induced cell death. [7][8][9] In vivo experiments support the results seen in cell lines. Capsaicin significantly slowed tumour growth in androgenindependent prostate cancer (PC-3) xenografts in mice.…”

Section: Discussionmentioning

confidence: 99%

Capsaicin may slow PSA doubling time: case report and literature review

Janković

Loblaw

Nam

2013

CUAJ

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Capsaicin is the main pungent component of chili peppers. Thisis the first case, to our knowledge, that describes prostatespecificantigen (PSA) stabilization in a patient with prostate cancer,who had biochemical failure after radiation therapy. A 66-year-old male underwent radiotherapy treatment for a T2b, Gleason7 (3+4) adenocarcinoma of the prostate, with a PSA level of13.3 ng/mL in April 2001. He had 3-dimensional conformal radiotherapyof 46 Gy in 23 fractions to the prostate and pelvis, and aprostate boost of 30 Gy in 15 fractions. Radiotherapy was completedin May 2001 and PSA nadired in January 2002 (0.57). Dueto the continued PSA rise, the patient was started on bicalutamide(50 mg orally, daily) and leuprolide acetate (1 dose of 22.5 mgintramuscularly) in July 2005 when PSA was 38.5 ng/mL. Due topoor tolerance of androgen ablation therapy, the patient discontinuedtreatment and started taking 2.5 mL of habaneros chilisauce, containing capsaicin, 1 to 2 times a week in April 2006.Prostate-specific antigen doubling time (PSAdt) increased from4 weeks before capsaicin to 7.3 months by October 2006. FromOctober 2006 until November 2007, the patient remained oncapsaicin (2.5 to 15 mL daily) and his PSA was stable (between11 to 14 ng/mL). By January 2008, his PSA rose to 22.3 and hehas maintained a PSAdt between 4 and 5 months, where it presentlyremains. Due to the patient’s continued PSA rise, he was restartedon bicalutamide (12.5 mg daily). Apart from PSA relapse, the patientremains free of signs or symptoms of recurrence.

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Apoptosis induction by dohevanil, a DHA substitutive analog of capsaicin, in MCF-7 cells

Cited by 31 publications

References 16 publications

Capsaicin-induced apoptosis in human breast cancer MCF-7 cells through caspase-independent pathway

Capsaicin-induced apoptosis in human breast cancer MCF-7 cells through caspase-independent pathway

Capsaicin causes cell-cycle arrest and apoptosis in ER-positive and -negative breast cancer cells by modulating the EGFR/HER-2 pathway

Capsaicin may slow PSA doubling time: case report and literature review

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