Mechanisms of radiotherapy resistance and radiosensitization strategies for esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC) is the sixth most common cause of cancer-related mortality worldwide, with more than half of them occurred in China. Radiotherapy (RT) has been widely used for treating ESCC. However, radiation-induced DNA damage response (DDR) can promote the release of cytokines and chemokines, and triggers inflammatory reactions and changes in the tumor microenvironment (TME), thereby inhibiting the immune function and causing the invasion and metastasis of ESCC. Radioresistance is the major cause of disease progression and mortality in cancer, and it is associated with heterogeneity. Therefore, a better understanding of the radioresistance mechanisms may generate more reversal strategies to improve the cure rates and survival periods of ESCC patients. We mainly summarized the possible mechanisms of radioresistance in order to reveal new targets for ESCC therapy. Then we summarized and compared the current strategies to reverse radioresistance.

BTG2 suppresses the growth and metastasis of cervical squamous cell carcinoma.

BACKGROUND: Cervical cancer is the fourth most common malignancy in women, of which cervical squamous cell carcinoma (CESC) is the main pathological type of cervical cancer. B-cell translocation gene 2 (BTG2) protein has been recognized as a tumor suppressor in several cancer types. However, BTG2 expression and molecular function in CESC are unknown. METHODS: In this study, we first assessed the expression of BTG2 in tumor tissue specimens from CESC patients using immunohistochemical staining and real-time quantitative PCR, and explored the relationship between BTG2 expression status and clinical manifestations. Next, we constructed BTG2 knockdown and overexpression CESC cell lines to observe the effects of BTG2 on CESC proliferation and metastasis at the cellular level. Finally, we employed a nude mouse xenograft tumor model in an in vivo experiment to observe the effect of BTG2 on tumorigenesis in vivo. RESULTS: The results showed that the expression of BTG2 protein was lower in CESC tissues than in normal tissues, and high BTG2 expression was associated with better survival in CESC patients versus CESC patients. The results of cellular assays confirm that overexpression of BTG2 inhibits the proliferation, migration and metastasis of CESC cells. Nude mouse xenograft tumor model showed that overexpression of BTG2 inhibited tumor growth in vivo, and conversely knockdown of BTG2 promoted tumor growth. CONCLUSION: In summary, our data suggest that BTG2 acts as a tumor suppressor in CESC and inhibits the growth and metastasis of CESC. BTG2 may serve as a potential prognostic marker in CESC and is expected to provide a therapeutic strategy for patients with CESC.