Growth suppression and induction of heat-shock protein-70 by 9-cis β-carotene in cervical dysplasia-derived cells

Toba, Toshinari; Shidoji, Yoshihiro; Fujii, Jun; Moriwaki, Hisataka; Muto, Yasutoshi; Suzuki, Takehiko; Ohishi, Nobuko; Yagi, Kazuichi

doi:10.1016/s0024-3205(97)00566-3

Cited by 22 publications

(13 citation statements)

References 13 publications

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“…Various agents and gene-transfection techniques have been reported to induce HSP70 expression in the stressed or unstressed conditions [13][14][15][16][17][18] as well as heat stress. For clinical applications, however, there are some problematic issues that require investigation, including too large amounts of dose, cytotoxicity, and induction efficiency.…”

mentioning

confidence: 99%

Preoperative Glutamine Administration Induces Heat-Shock Protein 70 Expression and Attenuates Cardiopulmonary Bypass–Induced Inflammatory Response by Regulating Nitric Oxide Synthase Activity

et al. 2002

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Background-Heat-shock protein 70 (HSP70) plays a major role in the pathophysiology of inflammation, and the induction of HSP70 before the onset of inflammation can reduce organ damage through a self-protective system. Glutamine is known to be an inducer of HSP70, and its preoperative administration seems useful in attenuating cardiopulmonary bypass (CPB)-induced inflammatory response. Methods and Results-Adult male Sprague-Dawley rats (group G, received 100 mg/kg of glutamine via the right jugular vein 3 times per day for 1 week and just before the initiation of CPB; group C served as control) underwent CPB (60 minutes, 100 mL/kg per minute, 34°C) and were killed 3 hours after the termination of CPB. Group G showed significantly lower plasma concentrations of interleukin-6 and interleukin-8 after CPB termination. Myocardial and respiratory damages were significantly attenuated in group G, as evidenced by Langendorff perfusion, respiratory index, and neutrophil adherence. HSP70 expressions in the heart, lung, and liver were detected only in group G before CPB and were markedly stronger in group G 3 hours after CPB termination. Although plasma nitrateϩnitrite concentrations were not significantly different between the groups, endothelial-constitutive nitric oxide synthase (NOS) activity was markedly preserved and inducible NOS activity was markedly attenuated in the tissues of group G. Conclusions-These results suggest that preoperative glutamine administration induces HSP70 expression before CPB and attenuates CPB-induced inflammation by regulating NOS activity, which may be a prospective management for conferring tolerance to CPB-induced inflammatory response through a self-protective mechanism. (Circulation. 2002; 106:2601-2607.)

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confidence: 99%

Preoperative Glutamine Administration Induces Heat-Shock Protein 70 Expression and Attenuates Cardiopulmonary Bypass–Induced Inflammatory Response by Regulating Nitric Oxide Synthase Activity

et al. 2002

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“…This observation clearly demonstrates a cellular response to β-carotene therapy in patients with GERD/Barrett's esophagus. Previous studies have confirmed that HSP70 induction by β-carotene therapy is associated with inhibition of cell growth in culture studies (Schwartz, 1990, Toba, 1997. Schwartz et al (1990) reported inhibition of proliferation of cultured human squamous cell assays (SK-MES lung carcinoma and SCC-25 oral carcinoma) and appearance of HSP70 within 1-2 hours of exposure to β-carotene.…”

Section: Discussionmentioning

confidence: 74%

“…Schwartz et al (1990) reported inhibition of proliferation of cultured human squamous cell assays (SK-MES lung carcinoma and SCC-25 oral carcinoma) and appearance of HSP70 within 1-2 hours of exposure to β-carotene. Likewise, Toba et al (1997) have demonstrated HSP70 induction by β-carotene in cervical dysplasia cells (CICCN-4 cells) associated with concentration-dependent suppression of cell growth through apoptosis. These authors have suggested that induction of HSP70 by β-carotene may be essential for inhibition of pre-malignant and malignant cell growth in cervical dysplasia (Toba, 1997).…”

Section: Discussionmentioning

confidence: 99%

“…Likewise, Toba et al (1997) have demonstrated HSP70 induction by β-carotene in cervical dysplasia cells (CICCN-4 cells) associated with concentration-dependent suppression of cell growth through apoptosis. These authors have suggested that induction of HSP70 by β-carotene may be essential for inhibition of pre-malignant and malignant cell growth in cervical dysplasia (Toba, 1997). Mechanistically, the resolution of Barrett's esophagus by β-carotene therapy points to a possible genomic reprogramming of the aberrant cells in the direction of normal differentiation.…”

Section: Discussionmentioning

confidence: 99%

“…There is also an increased HSP70 expression noted at the molecular level after β-carotene therapy, which might be cytoprotective against the acid damage and chemoprotective against early carcinogenic changes (Schwartz, 1990, Toba, 1997. Controlled double blinded clinical studies in larger number of patients are needed to confirm the efficacy of long-term β-carotene therapy in patients with Barrett's esophagus with dysplasia.…”

Section: Discussionmentioning

confidence: 99%

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Barrett's Esophagus and β-carotene Therapy: Symptomatic Improvement in GERD and Enhanced HSP70 Expression in Esophageal Mucosa

Dutta

Agrawal

Girotra

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Introduction: Epidemiological studies suggest a protective role for β-carotene with several malignancies. Esophageal adenocarcinoma frequently arises from Barrett's esophagus (BE). We postulated that β-carotene therapy maybe protective in BE. Materials and Method: We conducted a prospective study in which 25 mg of β-carotene was administered daily for six-months to six patients. Each patient underwent upper endoscopy before and after therapy and multiple mucosal biopsies were obtained. Additionally, patients completed a gastroesophageal reflux disease (GERD) symptoms questionnaire before and after therapy and severity score was calculated. To study the effect of β-carotene at molecular level, tissue extracts of the esophageal mucosal biopsy were subjected to assessment of heat-shock protein 70 (HSP70). Results: A significant (p<0.05) reduction in mean GERD symptoms severity score from 7.0±2.4 to 2.7±1.7 following β-carotene therapy was noted. Measurement of Barrett's segment also revealed a significant reduction in mean length after therapy. In fact, two patients had complete disappearance of intestinal metaplasia. Furthermore, marked enhancement of HSP70 expression was demonstrated in biopsy specimens from Barrett's epithelium in four cases that were tested. Conclusions: Longterm β-carotene therapy realizes amelioration of GERD symptoms along with restitution of the histological and molecular changes in esophageal mucosa of patients with BE, associated with concurrent increase in mucosal HSP70 expression.

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Chemoprevention of Lung Cancer

Cohen

Khuri

Tumors of the Chest

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Growth suppression and induction of heat-shock protein-70 by 9-cis β-carotene in cervical dysplasia-derived cells

Cited by 22 publications

References 13 publications

Preoperative Glutamine Administration Induces Heat-Shock Protein 70 Expression and Attenuates Cardiopulmonary Bypass–Induced Inflammatory Response by Regulating Nitric Oxide Synthase Activity

Preoperative Glutamine Administration Induces Heat-Shock Protein 70 Expression and Attenuates Cardiopulmonary Bypass–Induced Inflammatory Response by Regulating Nitric Oxide Synthase Activity

Barrett's Esophagus and β-carotene Therapy: Symptomatic Improvement in GERD and Enhanced HSP70 Expression in Esophageal Mucosa

Chemoprevention of Lung Cancer

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