SummaryBackgroundGastric cancer (GC) is one of the most common cancers in the world; however, chemoresistance greatly decreases the efficacy of therapy in gastric cancer. Long noncoding RNAs (IncRNAs) participate in a variety of biological processes, and we hypothesize that lncRNA HULC regulates the multidrug resistance in GC treatment.MethodsWe obtained GC tissue samples from 42 GC patients and detected the expression level of HULC in the plasma and tissues via qRT-PCR. The relationship between HULC expression and survival rate was confirmed by Kaplan-Meier survival analysis. We verified the expression of HULC in GC cell lines via qRT-PCR, and the function of HULC was detected via flow cytometry assay and CCK-8 assay.ResultsHULC was highly expressed in the plasma and tissues of the GC patients compared with controls, with HULC high expression indicating lower survival rate. HULC knockdown enhanced cisplatin-induced apoptosis in GC cells.ConclusionsOur results suggest that silencing lncRNA HULC could enhance chemotherapy induced apoptosis in GC cells, which could provide a novel approach for therapeutic strategies.

Nitidine chloride (NC) is a natural bioactive phytochemical alkaloid that has displayed anticancer activity in various types of cancer. However, no evidence has been reported for the direct effect of NC on CRC cell proliferation and apoptosis, and the underling mechanisms to be fully elucidated. The present study aimed to investigate the influence of NC on the apoptosis and proliferation of CRC cells. The viability and proliferation of CRC cells was measured by MTT assay and a [3H] thymidine uptake assay. Apoptosis was measured using a flow cytometric apoptosis assay and TUNEL staining. The expression levels of apoptotic-regulated proteins in addition to extracellular signal-regulated kinase (ERK) were measured by western blot analysis following stimulation with NC. The results indicated that NC inhibited the proliferation of HCT116 cells in a dose- and time-dependent manner. Additionally, apoptotic induction by NC treatment was confirmed. Furthermore, NC was demonstrated to significantly upregulate the expression of Bax, p53, cleaved caspase-3 and -9 and downregulate the expression of Bcl-2. Treatment with NC reduced the phosphorylation of ERK and by using an ERK inhibitor, U0126, the roles of NC in apoptotic induction and the inhibition of proliferation were further demonstrated. These results demonstrated that NC inhibited the proliferation and induced the apoptosis of CRC cells via the ERK signaling pathway.

Thyroid cancer (TC) is the most common endocrine malignancy. Lack of effective early diagnostic tools is one of the clinical obstacles for TC treatment. Thus, enhanced comprehension of the molecular changes in TC tumorigenesis is urgently needed to develop novel strategies for the diagnosis and treatment of TC. Long non-coding RNAs (lncRNAs) manage fundamental biochemical and cellular processes in tumorigenesis and development. One of the best-described lncRNAs, HOX transcript antisense RNA (HOTAIR), functions as a regulatory molecule in a wide variety of biological processes, and represses gene expression through recruitment of the chromatin modifying complex. However, the function of HOTAIR in TC remains unclear. In the current study, the expression of HOTAIR is elevated in TC and correlates with metastasis and poor prognosis. Furthermore, the expression of HOTAIR is significantly upregulated in human thyroid carcinoma cells compared with normal human thyroid cells. Furthermore, knockdown of HOTAIR significantly inhibited cell growth and invasion in TPC-1 and SW579 human thyroid carcinoma. In summary, HOTAIR is a promising novel biomarker in patients with TC.