Curcumin increases the sensitivity of Paclitaxel-resistant NSCLC cells to Paclitaxel through microRNA-30c-mediated MTA1 reduction.

Non-small-cell lung cancer is one of the most lethal cancers in the worldwide. Although Paclitaxel-based combinational therapies have long been used as a standard treatment in aggressive non-small-cell lung cancers, Paclitaxel resistance emerges as a major clinical problem. It has been demonstrated that Curcumin from Curcuma longa as a traditional Chinese medicine can inhibit cancer cell proliferation. However, the role of Curcumin in Paclitaxel-resistant non-small-cell lung cancer cells is not clear. In this study, we investigated the effect of Curcumin on the Paclitaxel-resistant non-small-cell lung cancer cells and found that Curcumin treatment markedly increased the sensitivity of Paclitaxel-resistant non-small-cell lung cancer cells to Paclitaxel. Mechanically, the study revealed that Curcumin could reduce the expression of metastasis-associated gene 1 (MTA1) gene through upregulation of microRNA-30c in Paclitaxel-resistant non-small-cell lung cancer cells. During the course, MTA1 reduction sensitized Paclitaxel-resistant non-small-cell lung cancer cells and enhanced the effect of Paclitaxel. Taken together, our studies indicate that Curcumin increases the sensitivity of Paclitaxel-resistant non-small-cell lung cancer cells to Paclitaxel through microRNA-30c-mediated MTA1 reduction. Curcumin might be a potential adjuvant for non-small-cell lung cancer patients during Paclitaxel treatment.

Expression of HIF-1α and P-gp in non-small cell lung cancer and the relationship with HPV infection.

The aim of the study was to study the expression of hypoxia-inducible factor-1α (HIF-1α) and P-glycoprotein (P-gp) and analyze its correlation with human papillomavirus (HPV) infection. From January, 2012 to May, 2014, 72 cases of non-small cell lung cancer (NSCLC) pathologic tissue samples were selected from the study group. Fifty-four lung benign lesions were selected to serve as the control group. HIF-1α and P-gp expression levels were detected using immunohistochemistry. PCR was used to detect the expression of HPV genome employing specific primers for HPV 16 and 18 types. The results showed that there was 47.2 and 63.9% positive HIF-1α and P-gp expression in the study group. No P-gp or HIF-1α expression was detected in the control group. The results established a positive correlation between the expression of HIF-1α and P-gp. In the study group, the expression and differentiation degree of HIF-1α was related to lymphatic metastasis. The HIF-1α expression in the well-differentiated samples was lower than that in the moderate or poorly differentiated samples. HIF-1α expression in patients with lymphatic metastasis was higher than in patients without metastasis. The expression rate of P-gp in adenocarcinoma was higher than that in squamous carcinoma. The detection rate of HPV DNA was 45.83 and 3.70% in the study and control groups, respectively. The HPV infection and differentiation degree had relevance to lymphatic metastasis in the study group. The HPV DNA detection rate in the well-differentiated samples was lower than that in the moderate or poorly differentiated samples. The HPV DNA detection rate in patients with lymphatic metastasis was higher than that in patients with no lymphatic metastasis. There was a close link between HIF-1α, P-gp expression and NSCLC occurrence, and the development of multidrug resistance. In conclusion, the detection of HIF-1α and P-gp expression can effectively predict drug resistance during chemotherapy in NSCLC, and these proteins can be used in drug prognosis.