Abstract
Qingjie Fuzheng granule (QFG) promotes cancer cell apoptosis and ameliorates intestinal mucosal damage caused by 5-fluorouracil. However, the antitumor role of QFG in colorectal cancer (CRC) progression remains unclear. In this study, the growth of HCT-8 and HCT116 cells incubated with various concentrations of QFG for 24 and 48 h was evaluated using MTT assays; their abilities of migration and invasion were investigated through wound healing and Transwell assays. The expression of lncRNA ANRIL, let-7a, and the TGF-β1/Smad signaling pathway components was assessed using real-time PCR and western blotting. The results elicited that QFG significantly suppressed the growth of HCT-8 and HCT116 cells; the half-maximal inhibitory concentrations (IC50) of QFG for HCT-8 and HCT116 cells for 48 h were 1.849 and 1.608 mg/mL, respectively. The abilities of wound healing, migration, and invasion of HCT-8 and HCT116 cells were dose-dependently decreased by QFG treatment for 24 h, respectively. QFG decreased the expression of lncRNA ANRIL, TGF-β1, phosphorylated (p)-Smad2/3, Smad4, and N-cadherin and upregulated the expression of let-7a in HCT-8 and HCT116 cells. Collectively, our data demonstrated that QFG inhibited the metastasis of CRC cells by regulating the lncRNA ANRIL/let-7a/TGF-β1/Smad axis, indicating that they might serve as an adjunctive medicine for CRC treatment.
Highlights
Colorectal cancer (CRC) is considered the second leading cause of cancer-related deaths [1]
Growth of HCT-8 and HCT116 Cells Was Inhibited by Qingjie Fuzheng granule (QFG). e growth-inhibitory effect of QFG on colorectal cancer (CRC) cell lines of HCT-8 and HCT116 was measured via MTT assays
To better evaluate the function of QFG in the metastasis of CRC, wound healing and Transwell assays were carried out on HCT-8 and HCT116 cells. e results of wound healing suggested that the doses of QFG at 0 to 2 mg/mL could significantly decrease the rate of wound healing in HCT-8 and HCT116 cells from 46.53 ± 4.66 to 6.69 ± 2.51% and 44.74 ± 1.29 to
Summary
Colorectal cancer (CRC) is considered the second leading cause of cancer-related deaths [1]. Clinical treatment options for metastatic colon cancer are limited, and this is the most common cause of high mortality rates for CRC [2]. Cancer cells undergo morphological changes called epithelial-mesenchymal transition (EMT). EMT leads to epithelial cells losing their adhesion and polarity properties and gaining a mesenchymal phenotype [3]. The cancer cells disseminate from the primary sites to distant organs [3]. Emerging evidence suggests that a family of long noncoding RNAs (lncRNAs) comprising >200 nucleotides with little to unknown protein-coding potential plays a vital role in cancer metastasis [4]
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