NAT1 is a critical prognostic biomarker and inhibits proliferation of colorectal cancer through modulation of PI3K/Akt/mTOR.

The aim of this study was to analyze the correlations between NAT1 and clinicopathological features of and prognosis in colorectal cancer (CRC). RNA sequencing data and clinical information were retrieved from The Cancer Genome Atlas database. Wilcoxon test, logistic regression and Kaplan-Meier method were used to estimate the association between NAT1 and prognosis in CRC. In vitro experiments were conducted to confirm the role of NAT1. NAT1 is significantly less expressed in CRC and independently associated with poor prognosis in CRC patients. The authors further confirmed that expression of NAT1 was significantly lower in SW116 colon cancer cells than in NCM460 cells. Overexpressed NAT1 obviously inhibited the growth of CRC cells by downregulating phosphorylation of the PI3K/Akt/mTOR signaling pathway. NAT1 may be a potential therapeutic target for CRC.

Lay abstract Colorectal cancer (CRC) is a common malignancy worldwide. Because of the limited understanding of the pathogenesis and prognostic factors associated with CRC, the treatment effect in CRC remains poor. In the present study, the authors demonstrate that NAT1 is significantly less expressed in CRC and independently associated with poor prognosis in CRC patients. NAT1 may exert antitumor activity by inhibiting phosphorylation of the PI3K/Akt/mTOR signaling pathway. These results suggest that NAT1 may be a prognostic factor in and therapeutic target for CRC.

Curcumin attenuates lncRNA H19­induced epithelial­mesenchymal transition in tamoxifen­resistant breast cancer cells.

The H19 long non­coding RNA is involved in the development of tamoxifen resistance in breast cancer. However, the relationship between H19 and the metastatic potential and treatment options for tamoxifen­resistant (TAMR) breast cancer is not completely understood. Curcumin inhibits cellular proliferation, migration and invasiveness in several cancer types, including pancreatic cancer, breast cancer and chronic myeloid leukemia. The present study aimed to investigate the role of H19 in MCF­7/TAMR cell epithelial­mesenchymal transition (EMT), migration and invasiveness, and to assess the ability of curcumin to inhibit H19­mediated effects. Reverse transcription­quantitative PCR and western blot analysis were conducted to detect the gene or protein expression. Cell Counting Kit­8, wound healing and Transwell invasion assays were performed to estimate the capabilities of cell viability, invasion and migration. H19 overexpression enhanced MCF­7/TAMR cell EMT, invasion and migration by upregulating Snail. Furthermore, curcumin notably decreased the expression levels of epithelial marker E­cadherin and markedly increased the expression levels of mesenchymal marker N­cadherin in MCF­7/TAMR cells compared with the control group. In addition, following treatment with curcumin for 48 h, H19 expression was decreased in a dose­dependent manner. Moreover, curcumin treatment for 48 h significantly attenuated H19­induced alterations in N­cadherin and E­cadherin expression levels. Curcumin also prevented H19­induced invasion and migration. The present study indicated that H19 may serve as a promoting factor of EMT, invasion and migration in MCF­7/TAMR cells, suggesting that curcumin may prevent H19­associated metastasis. Therefore, curcumin may serve as a promising therapeutic drug for patients with TAMR breast cancer.