Yafteh

Tumorigenesis is a complex and dynamic process. The microenvironment of tumors plays a pivotal role in the formation, initiation and progression of tumors. Studies on neoplastic developments focusing on tumor microenvironment events demonstrate its significance in promoting tumor progression. Prior to tumor metastasis, primary tumors secrete factors that create a proper metabolic environment for tumor metastasis. These conditions prepare the microenvironment for better and more efficient tumor growth. On the other hand, tumor cells continuously interact with the surrounding microenvironment, and targeting the tumor microenvironment can complement traditional treatment and improve the therapeutic outcomes for these malignancies. In the present article, the researchers attempt to highlight the importance of tumor microenvironment in tumorigenesis and tumor metabolism.

Cancer is a major and serious problem for human health. Despite the many advances in the field of treatment, it remains the biggest global medical challenge. The main barrier to treating this disease is a process called metastasis, which occurs in 90% of cancers.
According to World Health Statistics, breast cancer is among the three world's prevalent cancers and the second largest cause of cancer deaths in the world that is about 1.67 million people. Bone, liver, lung and brain are common organs for metastatic breast cancer. Proprietary processes and various molecules play a role in metastasis to each of these organs. The target microorganisms first cause the cancer cells to be present in these organs, and then the release of specific factors from cancer cells and their interaction with the target micro-environment results in the survival of these cells and the formation of metastasis. In this review article, we try to find out the key molecules of these mechanisms that can be considered as an appropriate therapeutic target for breast cancer by studying the mechanisms involved in metastatic breast cancer to target organs.

Background: Carvacrol is a natural monoterpene phenolic compound that has biological activities with therapeutic applications, and this study aimed to investigate the apoptotic effect of Carvacrol on the human breast cancer cell line MDA-MB-231.
Materials and Methods: After the preparation and cultivation of MDA-MB-231 cells, the IC50 value of Carvacrol on the cells was evaluated by the MTT assay method, and then the induction of apoptosis in the cell line treated with different concentrations of Carvacrol was observed by DAPI staining. The qPCR method was used to check the expression levels of Bax, P53, and Bcl-2 genes at the mRNA level. The results were analyzed using GraphPad Prism 9 software.
Results: The results showed that the cytotoxicity of Carvacrol against MDA-MB-231 cancer cells was dose-dependent at 24 (P=0.034) and 48 (P=0.041) hours. The IC50 of Carvacrol at 48 h was 154.2 μM. The MDA-MB-231 cells treated with Carvacrol showed induction of apoptosis from the mitochondrial pathway by increasing the expression of P53 and BAX genes and decreasing the expression of the anti-apoptotic Bcl-2 gene. In addition, the number of apoptotic cells with dense DNA increased significantly in the Carvacrol treatment group (P=0.001).
Conclusion: This study showed that treatment of the MDA-MB-231 cell line with Carvacrol can inhibit its growth and proliferation through the induction of apoptosis from the BAX/BCL-2 pathway. Considering the significant inhibitory effect of the treatment of cells with the Carvacrol compound, it seems that there is a suitable research field for using this compound in the control and treatment of breast cancer.