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Nihal Ahmad - One of the best experts on this subject based on the ideXlab platform.

  • Prevention of short-term ultraviolet B radiation-mediated damages by resveratrol in SKH-1 hairless mice.
    Toxicology and applied pharmacology, 2003
    Co-Authors: Farrukh Afaq, Vaqar M. Adhami, Nihal Ahmad
    Abstract:

    Abstract Nonmelanoma skin cancer is the most common cancer among humans and solar UV radiation, particularly its UVB component (290–320 nm), is its major cause. One way to reduce the occurrence of the cancer is via the use of substances (often antioxidants) termed “ photochemopreventive agents ”. Resveratrol ( trans -3,4′,5-trihydroxystilbene), a phytoalexin found in grapes, Nuts, Fruits, and red wine, is a potent antioxidant with strong anti-inflammatory and antiproliferative properties. This study was designed to examine whether resveratrol possesses the potential to ameliorate the damages caused by short-term UVB exposure to mouse skin. Single topical application of resveratrol (25 μmol/0.2 ml acetone per mouse) to SKH-1 hairless mice was found to result in significant inhibition of UVB (180 mJ/cm 2 )-mediated increase in bifold skin thickness and skin edema. The resveratrol treatment to mouse skin was also found to result in significant inhibition of UVB-mediated induction of cyclooxygenase and ornithine decarboxylase (ODC) enzyme activities and protein expression of ODC, which are well-established markers for tumor promotion. We also observed that resveratrol inhibits UVB-mediated increased level of lipid peroxidation, a marker of oxidative stress. Taken together, our results suggest that resveratrol may afford substantial protection against the damages caused by UVB exposure, and these protective effects may be mediated via its antioxidant properties.

  • resveratrol causes waf 1 p21 mediated g1 phase arrest of cell cycle and induction of apoptosis in human epidermoid carcinoma a431 cells
    Clinical Cancer Research, 2001
    Co-Authors: Nihal Ahmad, Farrukh Afaq, Vaqar M. Adhami, Denise K Feyes, Hasan Mukhtar
    Abstract:

    Resveratrol ( trans -3,4′,5,-trihydroxystilbene), a phytoalexin found in grapes, Nuts, Fruits, and red wine, is a potent antioxidant with cancer-preventive properties. The mechanism by which resveratrol imparts cancer chemopreventive effects is not clearly defined. Here, we demonstrate that resveratrol, via modulations in cyclin-dependent kinase (cdk) inhibitor-cyclin-cdk machinery, results in a G 1 -phase arrest of the cell cycle followed by apoptosis of human epidermoid carcinoma (A431) cells. Resveratrol treatment (1–50 μm for 24 h) of A431 cells resulted in a dose-dependent ( a ) inhibition of cell growth as shown by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, ( b ) G 1 -phase arrest of the cell cycle as shown by DNA cell cycle analysis, and ( c ) induction of apoptosis as assessed by ELISA. The immunoblot analysis revealed that resveratrol treatment causes a dose- and time-dependent ( a ) induction of WAF1/p21; ( b ) decrease in the protein expressions of cyclin D1, cyclin D2, and cyclin E; and ( c ) decrease in the protein expressions of cdk2, cdk4, and cdk6. Resveratrol treatment was also found to result in a dose- and time-dependent decrease in kinase activities associated with all of the cdks examined. Taken together, our study suggests that resveratrol treatment of the cells causes an induction of WAF1/p21 that inhibits cyclin D1/D2-cdk6, cyclin D1/D2-cdk4, and cyclin E-cdk2 complexes, thereby imposing an artificial checkpoint at the G 1 →S transition of the cell cycle. This series of events results in a G 1 -phase arrest of the cell cycle, which is an irreversible process that ultimately results in the apoptotic death of cancer cells. To our knowledge, this is the first systematic study showing the involvement of each component of cdk inhibitor-cyclin-cdk machinery during cell cycle arrest and apoptosis of cancer cells by resveratrol.

  • Resveratrol causes WAF-1/p21-mediated G(1)-phase arrest of cell cycle and induction of apoptosis in human epidermoid carcinoma A431 cells.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2001
    Co-Authors: Nihal Ahmad, Farrukh Afaq, Vaqar M. Adhami, Denise K Feyes, Hasan Mukhtar
    Abstract:

    Resveratrol (trans-3,4',5,-trihydroxystilbene), a phytoalexin found in grapes, Nuts, Fruits, and red wine, is a potent antioxidant with cancer-preventive properties. The mechanism by which resveratrol imparts cancer chemopreventive effects is not clearly defined. Here, we demonstrate that resveratrol, via modulations in cyclin-dependent kinase (cdk) inhibitor-cyclin-cdk machinery, results in a G(1)-phase arrest of the cell cycle followed by apoptosis of human epidermoid carcinoma (A431) cells. Resveratrol treatment (1-50 microM for 24 h) of A431 cells resulted in a dose-dependent (a) inhibition of cell growth as shown by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, (b) G(1)-phase arrest of the cell cycle as shown by DNA cell cycle analysis, and (c) induction of apoptosis as assessed by ELISA. The immunoblot analysis revealed that resveratrol treatment causes a dose- and time-dependent (a) induction of WAF1/p21; (b) decrease in the protein expressions of cyclin D1, cyclin D2, and cyclin E; and (c) decrease in the protein expressions of cdk2, cdk4, and cdk6. Resveratrol treatment was also found to result in a dose- and time-dependent decrease in kinase activities associated with all of the cdks examined. Taken together, our study suggests that resveratrol treatment of the cells causes an induction of WAF1/p21 that inhibits cyclin D1/D2-cdk6, cyclin D1/D2-cdk4, and cyclin E-cdk2 complexes, thereby imposing an artificial checkpoint at the G(1)-->S transition of the cell cycle. This series of events results in a G(1)-phase arrest of the cell cycle, which is an irreversible process that ultimately results in the apoptotic death of cancer cells. To our knowledge, this is the first systematic study showing the involvement of each component of cdk inhibitor-cyclin-cdk machinery during cell cycle arrest and apoptosis of cancer cells by resveratrol.

Farrukh Afaq - One of the best experts on this subject based on the ideXlab platform.

  • Prevention of short-term ultraviolet B radiation-mediated damages by resveratrol in SKH-1 hairless mice.
    Toxicology and applied pharmacology, 2003
    Co-Authors: Farrukh Afaq, Vaqar M. Adhami, Nihal Ahmad
    Abstract:

    Abstract Nonmelanoma skin cancer is the most common cancer among humans and solar UV radiation, particularly its UVB component (290–320 nm), is its major cause. One way to reduce the occurrence of the cancer is via the use of substances (often antioxidants) termed “ photochemopreventive agents ”. Resveratrol ( trans -3,4′,5-trihydroxystilbene), a phytoalexin found in grapes, Nuts, Fruits, and red wine, is a potent antioxidant with strong anti-inflammatory and antiproliferative properties. This study was designed to examine whether resveratrol possesses the potential to ameliorate the damages caused by short-term UVB exposure to mouse skin. Single topical application of resveratrol (25 μmol/0.2 ml acetone per mouse) to SKH-1 hairless mice was found to result in significant inhibition of UVB (180 mJ/cm 2 )-mediated increase in bifold skin thickness and skin edema. The resveratrol treatment to mouse skin was also found to result in significant inhibition of UVB-mediated induction of cyclooxygenase and ornithine decarboxylase (ODC) enzyme activities and protein expression of ODC, which are well-established markers for tumor promotion. We also observed that resveratrol inhibits UVB-mediated increased level of lipid peroxidation, a marker of oxidative stress. Taken together, our results suggest that resveratrol may afford substantial protection against the damages caused by UVB exposure, and these protective effects may be mediated via its antioxidant properties.

  • resveratrol causes waf 1 p21 mediated g1 phase arrest of cell cycle and induction of apoptosis in human epidermoid carcinoma a431 cells
    Clinical Cancer Research, 2001
    Co-Authors: Nihal Ahmad, Farrukh Afaq, Vaqar M. Adhami, Denise K Feyes, Hasan Mukhtar
    Abstract:

    Resveratrol ( trans -3,4′,5,-trihydroxystilbene), a phytoalexin found in grapes, Nuts, Fruits, and red wine, is a potent antioxidant with cancer-preventive properties. The mechanism by which resveratrol imparts cancer chemopreventive effects is not clearly defined. Here, we demonstrate that resveratrol, via modulations in cyclin-dependent kinase (cdk) inhibitor-cyclin-cdk machinery, results in a G 1 -phase arrest of the cell cycle followed by apoptosis of human epidermoid carcinoma (A431) cells. Resveratrol treatment (1–50 μm for 24 h) of A431 cells resulted in a dose-dependent ( a ) inhibition of cell growth as shown by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, ( b ) G 1 -phase arrest of the cell cycle as shown by DNA cell cycle analysis, and ( c ) induction of apoptosis as assessed by ELISA. The immunoblot analysis revealed that resveratrol treatment causes a dose- and time-dependent ( a ) induction of WAF1/p21; ( b ) decrease in the protein expressions of cyclin D1, cyclin D2, and cyclin E; and ( c ) decrease in the protein expressions of cdk2, cdk4, and cdk6. Resveratrol treatment was also found to result in a dose- and time-dependent decrease in kinase activities associated with all of the cdks examined. Taken together, our study suggests that resveratrol treatment of the cells causes an induction of WAF1/p21 that inhibits cyclin D1/D2-cdk6, cyclin D1/D2-cdk4, and cyclin E-cdk2 complexes, thereby imposing an artificial checkpoint at the G 1 →S transition of the cell cycle. This series of events results in a G 1 -phase arrest of the cell cycle, which is an irreversible process that ultimately results in the apoptotic death of cancer cells. To our knowledge, this is the first systematic study showing the involvement of each component of cdk inhibitor-cyclin-cdk machinery during cell cycle arrest and apoptosis of cancer cells by resveratrol.

  • Resveratrol causes WAF-1/p21-mediated G(1)-phase arrest of cell cycle and induction of apoptosis in human epidermoid carcinoma A431 cells.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2001
    Co-Authors: Nihal Ahmad, Farrukh Afaq, Vaqar M. Adhami, Denise K Feyes, Hasan Mukhtar
    Abstract:

    Resveratrol (trans-3,4',5,-trihydroxystilbene), a phytoalexin found in grapes, Nuts, Fruits, and red wine, is a potent antioxidant with cancer-preventive properties. The mechanism by which resveratrol imparts cancer chemopreventive effects is not clearly defined. Here, we demonstrate that resveratrol, via modulations in cyclin-dependent kinase (cdk) inhibitor-cyclin-cdk machinery, results in a G(1)-phase arrest of the cell cycle followed by apoptosis of human epidermoid carcinoma (A431) cells. Resveratrol treatment (1-50 microM for 24 h) of A431 cells resulted in a dose-dependent (a) inhibition of cell growth as shown by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, (b) G(1)-phase arrest of the cell cycle as shown by DNA cell cycle analysis, and (c) induction of apoptosis as assessed by ELISA. The immunoblot analysis revealed that resveratrol treatment causes a dose- and time-dependent (a) induction of WAF1/p21; (b) decrease in the protein expressions of cyclin D1, cyclin D2, and cyclin E; and (c) decrease in the protein expressions of cdk2, cdk4, and cdk6. Resveratrol treatment was also found to result in a dose- and time-dependent decrease in kinase activities associated with all of the cdks examined. Taken together, our study suggests that resveratrol treatment of the cells causes an induction of WAF1/p21 that inhibits cyclin D1/D2-cdk6, cyclin D1/D2-cdk4, and cyclin E-cdk2 complexes, thereby imposing an artificial checkpoint at the G(1)-->S transition of the cell cycle. This series of events results in a G(1)-phase arrest of the cell cycle, which is an irreversible process that ultimately results in the apoptotic death of cancer cells. To our knowledge, this is the first systematic study showing the involvement of each component of cdk inhibitor-cyclin-cdk machinery during cell cycle arrest and apoptosis of cancer cells by resveratrol.

Magdalena S Rosell - One of the best experts on this subject based on the ideXlab platform.

  • Health effects of vegetarian and vegan diets
    The Proceedings of the Nutrition Society, 2006
    Co-Authors: Timothy J. Key, Paul N. Appleby, Magdalena S Rosell
    Abstract:

    Vegetarian diets do not contain meat, poultry or fish; vegan diets further exclude dairy products and eggs. Vegetarian and vegan diets can vary widely, but the empirical evidence largely relates to the nutritional content and health effects of the average diet of well-educated vegetarians living in Western countries, together with some information on vegetarians in nonWestern countries. In general, vegetarian diets provide relatively large amounts of cereals, pulses, Nuts, Fruits and vegetables. In terms of nutrients, vegetarian diets are usually rich in carbohydrates, n-6 fatty acids, dietary fibre, carotenoids, folic acid, vitamin C, vitamin E and Mg, and relatively low in protein, saturated fat, long-chain n-3 fatty acids, retinol, vitamin B12 and Zn; vegans may have particularly low intakes of vitamin B12 and low intakes of Ca. Crosssectional studies of vegetarians and vegans have shown that on average they have a relatively low BMI and a low plasma cholesterol concentration; recent studies have also shown higher plasma homocysteine concentrations than in non-vegetarians. Cohort studies of vegetarians have shown a moderate reduction in mortality from IHD but little difference in other major causes of death or all-cause mortality in comparison with health-conscious non-vegetarians from the same population. Studies of cancer have not shown clear differences in cancer rates between vegetarians and non-vegetarians. More data are needed, particularly on the health of vegans and on the possible impacts on health of low intakes of long-chain n-3 fatty acids and vitamin B12. Overall, the data suggest that the health of Western vegetarians is good and similar to that of comparable non-vegetarians.

Hasan Mukhtar - One of the best experts on this subject based on the ideXlab platform.

  • resveratrol causes waf 1 p21 mediated g1 phase arrest of cell cycle and induction of apoptosis in human epidermoid carcinoma a431 cells
    Clinical Cancer Research, 2001
    Co-Authors: Nihal Ahmad, Farrukh Afaq, Vaqar M. Adhami, Denise K Feyes, Hasan Mukhtar
    Abstract:

    Resveratrol ( trans -3,4′,5,-trihydroxystilbene), a phytoalexin found in grapes, Nuts, Fruits, and red wine, is a potent antioxidant with cancer-preventive properties. The mechanism by which resveratrol imparts cancer chemopreventive effects is not clearly defined. Here, we demonstrate that resveratrol, via modulations in cyclin-dependent kinase (cdk) inhibitor-cyclin-cdk machinery, results in a G 1 -phase arrest of the cell cycle followed by apoptosis of human epidermoid carcinoma (A431) cells. Resveratrol treatment (1–50 μm for 24 h) of A431 cells resulted in a dose-dependent ( a ) inhibition of cell growth as shown by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, ( b ) G 1 -phase arrest of the cell cycle as shown by DNA cell cycle analysis, and ( c ) induction of apoptosis as assessed by ELISA. The immunoblot analysis revealed that resveratrol treatment causes a dose- and time-dependent ( a ) induction of WAF1/p21; ( b ) decrease in the protein expressions of cyclin D1, cyclin D2, and cyclin E; and ( c ) decrease in the protein expressions of cdk2, cdk4, and cdk6. Resveratrol treatment was also found to result in a dose- and time-dependent decrease in kinase activities associated with all of the cdks examined. Taken together, our study suggests that resveratrol treatment of the cells causes an induction of WAF1/p21 that inhibits cyclin D1/D2-cdk6, cyclin D1/D2-cdk4, and cyclin E-cdk2 complexes, thereby imposing an artificial checkpoint at the G 1 →S transition of the cell cycle. This series of events results in a G 1 -phase arrest of the cell cycle, which is an irreversible process that ultimately results in the apoptotic death of cancer cells. To our knowledge, this is the first systematic study showing the involvement of each component of cdk inhibitor-cyclin-cdk machinery during cell cycle arrest and apoptosis of cancer cells by resveratrol.

  • Resveratrol causes WAF-1/p21-mediated G(1)-phase arrest of cell cycle and induction of apoptosis in human epidermoid carcinoma A431 cells.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2001
    Co-Authors: Nihal Ahmad, Farrukh Afaq, Vaqar M. Adhami, Denise K Feyes, Hasan Mukhtar
    Abstract:

    Resveratrol (trans-3,4',5,-trihydroxystilbene), a phytoalexin found in grapes, Nuts, Fruits, and red wine, is a potent antioxidant with cancer-preventive properties. The mechanism by which resveratrol imparts cancer chemopreventive effects is not clearly defined. Here, we demonstrate that resveratrol, via modulations in cyclin-dependent kinase (cdk) inhibitor-cyclin-cdk machinery, results in a G(1)-phase arrest of the cell cycle followed by apoptosis of human epidermoid carcinoma (A431) cells. Resveratrol treatment (1-50 microM for 24 h) of A431 cells resulted in a dose-dependent (a) inhibition of cell growth as shown by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, (b) G(1)-phase arrest of the cell cycle as shown by DNA cell cycle analysis, and (c) induction of apoptosis as assessed by ELISA. The immunoblot analysis revealed that resveratrol treatment causes a dose- and time-dependent (a) induction of WAF1/p21; (b) decrease in the protein expressions of cyclin D1, cyclin D2, and cyclin E; and (c) decrease in the protein expressions of cdk2, cdk4, and cdk6. Resveratrol treatment was also found to result in a dose- and time-dependent decrease in kinase activities associated with all of the cdks examined. Taken together, our study suggests that resveratrol treatment of the cells causes an induction of WAF1/p21 that inhibits cyclin D1/D2-cdk6, cyclin D1/D2-cdk4, and cyclin E-cdk2 complexes, thereby imposing an artificial checkpoint at the G(1)-->S transition of the cell cycle. This series of events results in a G(1)-phase arrest of the cell cycle, which is an irreversible process that ultimately results in the apoptotic death of cancer cells. To our knowledge, this is the first systematic study showing the involvement of each component of cdk inhibitor-cyclin-cdk machinery during cell cycle arrest and apoptosis of cancer cells by resveratrol.

Vaqar M. Adhami - One of the best experts on this subject based on the ideXlab platform.

  • Prevention of short-term ultraviolet B radiation-mediated damages by resveratrol in SKH-1 hairless mice.
    Toxicology and applied pharmacology, 2003
    Co-Authors: Farrukh Afaq, Vaqar M. Adhami, Nihal Ahmad
    Abstract:

    Abstract Nonmelanoma skin cancer is the most common cancer among humans and solar UV radiation, particularly its UVB component (290–320 nm), is its major cause. One way to reduce the occurrence of the cancer is via the use of substances (often antioxidants) termed “ photochemopreventive agents ”. Resveratrol ( trans -3,4′,5-trihydroxystilbene), a phytoalexin found in grapes, Nuts, Fruits, and red wine, is a potent antioxidant with strong anti-inflammatory and antiproliferative properties. This study was designed to examine whether resveratrol possesses the potential to ameliorate the damages caused by short-term UVB exposure to mouse skin. Single topical application of resveratrol (25 μmol/0.2 ml acetone per mouse) to SKH-1 hairless mice was found to result in significant inhibition of UVB (180 mJ/cm 2 )-mediated increase in bifold skin thickness and skin edema. The resveratrol treatment to mouse skin was also found to result in significant inhibition of UVB-mediated induction of cyclooxygenase and ornithine decarboxylase (ODC) enzyme activities and protein expression of ODC, which are well-established markers for tumor promotion. We also observed that resveratrol inhibits UVB-mediated increased level of lipid peroxidation, a marker of oxidative stress. Taken together, our results suggest that resveratrol may afford substantial protection against the damages caused by UVB exposure, and these protective effects may be mediated via its antioxidant properties.

  • resveratrol causes waf 1 p21 mediated g1 phase arrest of cell cycle and induction of apoptosis in human epidermoid carcinoma a431 cells
    Clinical Cancer Research, 2001
    Co-Authors: Nihal Ahmad, Farrukh Afaq, Vaqar M. Adhami, Denise K Feyes, Hasan Mukhtar
    Abstract:

    Resveratrol ( trans -3,4′,5,-trihydroxystilbene), a phytoalexin found in grapes, Nuts, Fruits, and red wine, is a potent antioxidant with cancer-preventive properties. The mechanism by which resveratrol imparts cancer chemopreventive effects is not clearly defined. Here, we demonstrate that resveratrol, via modulations in cyclin-dependent kinase (cdk) inhibitor-cyclin-cdk machinery, results in a G 1 -phase arrest of the cell cycle followed by apoptosis of human epidermoid carcinoma (A431) cells. Resveratrol treatment (1–50 μm for 24 h) of A431 cells resulted in a dose-dependent ( a ) inhibition of cell growth as shown by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, ( b ) G 1 -phase arrest of the cell cycle as shown by DNA cell cycle analysis, and ( c ) induction of apoptosis as assessed by ELISA. The immunoblot analysis revealed that resveratrol treatment causes a dose- and time-dependent ( a ) induction of WAF1/p21; ( b ) decrease in the protein expressions of cyclin D1, cyclin D2, and cyclin E; and ( c ) decrease in the protein expressions of cdk2, cdk4, and cdk6. Resveratrol treatment was also found to result in a dose- and time-dependent decrease in kinase activities associated with all of the cdks examined. Taken together, our study suggests that resveratrol treatment of the cells causes an induction of WAF1/p21 that inhibits cyclin D1/D2-cdk6, cyclin D1/D2-cdk4, and cyclin E-cdk2 complexes, thereby imposing an artificial checkpoint at the G 1 →S transition of the cell cycle. This series of events results in a G 1 -phase arrest of the cell cycle, which is an irreversible process that ultimately results in the apoptotic death of cancer cells. To our knowledge, this is the first systematic study showing the involvement of each component of cdk inhibitor-cyclin-cdk machinery during cell cycle arrest and apoptosis of cancer cells by resveratrol.

  • Resveratrol causes WAF-1/p21-mediated G(1)-phase arrest of cell cycle and induction of apoptosis in human epidermoid carcinoma A431 cells.
    Clinical cancer research : an official journal of the American Association for Cancer Research, 2001
    Co-Authors: Nihal Ahmad, Farrukh Afaq, Vaqar M. Adhami, Denise K Feyes, Hasan Mukhtar
    Abstract:

    Resveratrol (trans-3,4',5,-trihydroxystilbene), a phytoalexin found in grapes, Nuts, Fruits, and red wine, is a potent antioxidant with cancer-preventive properties. The mechanism by which resveratrol imparts cancer chemopreventive effects is not clearly defined. Here, we demonstrate that resveratrol, via modulations in cyclin-dependent kinase (cdk) inhibitor-cyclin-cdk machinery, results in a G(1)-phase arrest of the cell cycle followed by apoptosis of human epidermoid carcinoma (A431) cells. Resveratrol treatment (1-50 microM for 24 h) of A431 cells resulted in a dose-dependent (a) inhibition of cell growth as shown by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, (b) G(1)-phase arrest of the cell cycle as shown by DNA cell cycle analysis, and (c) induction of apoptosis as assessed by ELISA. The immunoblot analysis revealed that resveratrol treatment causes a dose- and time-dependent (a) induction of WAF1/p21; (b) decrease in the protein expressions of cyclin D1, cyclin D2, and cyclin E; and (c) decrease in the protein expressions of cdk2, cdk4, and cdk6. Resveratrol treatment was also found to result in a dose- and time-dependent decrease in kinase activities associated with all of the cdks examined. Taken together, our study suggests that resveratrol treatment of the cells causes an induction of WAF1/p21 that inhibits cyclin D1/D2-cdk6, cyclin D1/D2-cdk4, and cyclin E-cdk2 complexes, thereby imposing an artificial checkpoint at the G(1)-->S transition of the cell cycle. This series of events results in a G(1)-phase arrest of the cell cycle, which is an irreversible process that ultimately results in the apoptotic death of cancer cells. To our knowledge, this is the first systematic study showing the involvement of each component of cdk inhibitor-cyclin-cdk machinery during cell cycle arrest and apoptosis of cancer cells by resveratrol.