Effects Of Carvacrol On Breast Cancer And Cervical Cancer And The Possible Mechanism

Background and purposeBreast cancer and cervical cancer is the first and the second cause of death in cancer that is related to women in the world.Now the common used treatment includes surgical treatment,radiotherapy and chemotherapy,but in advanced stage most patients lose the timing of surgical treatments,traditional chemotherapy drugs have more adverse reactions,Therefor,we need to find a new type of chemotherapy drugs that is used to treat breast cancer and cervical cancer.The effects of Chinese herbal extracts have been extensively studied.There have been many studies on the antimicrobial,fungicidal,anti carcinogenic,and antioxidant activities of Carvacrol.The present study aimed to explore the effect and the possible mechanism of Carvacrol on MCF-7 cells of breast cancer and HELA cells of cervical cancer,and to provide new chemotherapy drugs and theoretical basis for the treatment of breast cancer cells and cervical cancer cells.MethodsMCF-7 cells of breast cancer and HELA cells of cervical cancer were cultured,and the cancer cells that grew well were taken for experiments.MCF-7 cell of breast cancer and HELA cells of cervical cancer were spread into 96-well microtiter plates or 6-well plate and waited for 24 hours to adhere to the wall,The cells are treated without(the negative control)or with test different concentrations of carvacrol(experimental group)Cell Counting Kit-8 were used to detect the viability and proliferation of MCF-7 cells of breast cancer and HELA cells of cervical cancer.In Flow cytometry,apoptosis rates was detect from MCF-7 cells of breast cancer and HELA cells of cervical cancer.the change of migration ability of MCF-7 cells of breast cancer and HELA cells of cervical cancer transfected or not was investigated by wound healing.Western Bolt methods were used to detect the expression of MAPK family in the MCF-7 cells of breast cancer and HELA cells of cervical cancer.Results1.Results of Cell Counting Kit-8(CCK-8):Cervical cancer HELA cells and breast cancer MCF-7 cells were divided into experimental group(150umol/1,250umol/l,350umol/l,450umol/l,550umol/l,650umol/l)and blank drug concentration control group according to an average of 104-105 cells spread into 96-well microtiter plates,and grown for additional 24 h prior to the CCK8 experiment.The results showed that Carvacrol significantly inhibited HELA cells in cervical cancer and MCF-7 cells in breast cancer,and the cell survival rate was negatively correlated with the drug concentration.2.Results of apoptosis rates:Cervical cancer HELA cells and breast cancer MCF-7 cells were divided into experimental group(150umol/l,250umol/l,350umol/l,450umol/l)and blank drug concentration control group according to 5 ×105 cells laid in 6-well plate The degree of apoptosis was detected by flow cytometry 24 hours after drug action.The results showed that Carvacrol can induce apoptosis of HELA cells and MCF-7 cells.3.Wound healing results:HELA cells of cervical cancer and MCF-7 cells of breast cancer according to the 5×105 spread into 6-well plate,divided into experimental group(150umol/l,250umol/l,350umol/l,450umol/l)drug concentration and blank control group,24 hours after the drug photographed under a microscope,the results showed that in carvacrol 24 hours after HELA mobility has no obvious change,and MCF-7 cell migration rate was significantly suppressed.4.Western Blot results:HELA cells of cervical cancer and MCF-7 cells of breast cancer were divided into experimental group(150umol/l,250umol/l,350umol/l,450umol/l)and blank drug concentration control group according to 5 ×105 in 6-well plate,and grown for additional 24 h prior to Western Blot.In MCF-7 cells of breast cancer,Results showed that there were no significant differences in ERK1/2,JNK and P38 in MCF-7 cells treated with Carvacrol,but the expression levels of P-ERK1/2,P-JNK and P-P38 were significantly decreased and negatively correlated with drug concentration Similarly,there was no significant difference in the ERK1/2,JNK and P38 in HELA cells after the action of Carvacrol.However,the expression level of P-ERK1/2,P-JNK,and P-P38 first increased and then decreased.ConclusionsWithin a certain concentration range,Carvacrol inhibits the proliferation of MCF-7 cells in breast cancer,promotes their apoptosis and inhibites cell migration.The mechanism may be achieved by regulating the expression level of certain proteins in MAPK family.Within a certain range,Carvacrol promotes the apoptosis of HELA cells in cervical cancer and inhibites cell proliferation,The mechanism may be achieved by regulating the expression level of certain proteins in MAPK family.