Gastric cancer (GC) is one of the leading causes of cancer death in the world. The role of histone deacetylase 4 (HDAC4) in specific cell and tissue types has been identified. However, its biological roles in the development of gastric cancer remain largely unexplored. Quantitative real time PCR (qRT-PCR) and western blot were used to analyze the expression of HDAC4 in the clinical samples. siRNA and overexpression of HDAC4 and siRNA p21 were used to study functional effects in a proliferation, a colony formation, a adenosine 5′-triphosphate (ATP) assay and reactive oxygen species(ROS) generation, cell cycle, cell apoptosis rates, and autophagy assays. HDAC4 was up-regulated in gastric cancer tissues and several gastric cancer cell lines. The proliferation, colony formation ability and ATP level were enhanced in HDAC4 overexpression SGC-7901 cells, but inhibited in HDAC4 knockdown SGC-7901 cells. HDAC4 knockdown led to G0/G1 phase cell arrest and caused apoptosis and ROS increase. Moreover, HDAC4 was found to inhibit p21 expression in gastric cancer SGC-7901 cells. p21 knockdown dramatically attenuated cell proliferation inhibition, cell cycle arrest, cell apoptosis promotion and autophagy up-regulation in HDAC4-siRNA SGC-7901 cells. We demonstrated that HDAC4 promotes gastric cancer cell progression mediated through the repression of p21. Our results provide an experimental basis for understanding the pro-tumor mechanism of HDAC4 as treatment for gastric cancer.

Ion channels are involved in regulating cell proliferation and apoptosis (programed cell death). Since increased cellular proliferation and inhibition of apoptosis are characteristic features of tumorigenesis, targeting ion channels is a promising strategy for treating cancer. CLC-3 is a member of the voltage-gated chloride channel superfamily and is expressed in many cancer cells. In the plasma membrane, CLC-3 functions as a chloride channel and is associated with cell proliferation and apoptosis. CLC-3 is also located in intracellular compartments, contributing to their acidity, which increases sequestration of drugs and leads to chemotherapy drug resistance. In this review, we summarize the recent findings concerning the involvement of CLC-3 in cancer and explore its potential in cancer therapy.

Paeoniflorin (PF) exhibits tumor suppressive functions in a variety of human cancers. However, the function of PF and molecular mechanism in colorectal cancer are elusive. In the present study, we investigated whether PF could exert its antiproliferative activity, anti-migration, and anti-invasive function in colorectal cancer cells. We found that PF inhibited cell growth and induced apoptosis and blocked cell cycle progression in the G0/G1 phase in colorectal cancer cells. Moreover, we found that PF suppressed cell migration and invasion in colorectal cancer cells. FoxM1 has been reported to play an important oncogenic role in human cancers. We also determine whether PF inhibited the expression of FoxM1, leading to its anti-cancer activity. We found that PF treatment in colorectal cancer cells resulted in down-regulation of FoxM1. The rescue experiments showed that overexpression of FoxM1 abrogated the tumor suppressive function induced by PF treatment. Notably, depletion of FoxM1 promoted the anti-tumor activity of PF in colorectal cancer cells. Therefore, inhibition of FoxM1 could participate in the anti-tumor activity of PF in colorectal cancer cells.

PurposeThis study aimed to evaluate the short- and long-term outcomes of laparoscopic hepatectomy (LH) for colorectal liver metastases (CRLM) in elderly patients.Patients and methodsBetween January 2009 and January 2016, LH was performed for 241 consecutive patients who were ≥60 years old and had CRLM. Based on their age at the LH, the patients were divided into an elderly group (≥70 years old, 78 patients) and a middle-aged group (60–69 years old, 163 patients). The short- and long-term outcomes were compared between the two groups.ResultsCompared to the middle-aged group, the elderly group had higher values for Charlson comorbidity index, proportion of preoperative chemotherapy, and American Society of Anesthesiologists score. No other significant differences were observed in the preoperative characteristics. The elderly group had a higher conversion rate, compared to the middle-aged group, although no significant differences were observed in the surgical procedures, surgical times, intraoperative blood losses, numbers and severities of postoperative 90-day complications, postoperative 90-day mortality rates, pathology results, and other short-term outcomes. Long-term follow-up revealed similar rates of recurrence, disease-free survival, and overall survival in the two groups. Multivariable analysis revealed that age did not independently predict overall survival or disease-free survival.ConclusionSimilar short- and long-term outcomes were observed after LH for CRLM in elderly and middle-aged patients. Thus, advanced age is not a contraindication for LH treatment in this setting.

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Immunodominant T cell responses are important for protection against virus challenge. However, studies screening for the immunodominant T cell responses and following their kinetics in acute Hantaan virus (HTNV) infection are very limited. Herein, the HTNV nucleocapsid protein-specific T cell responses were longitudinally screened in 15 patients with acute HTNV infection, eight of whom had a particularly severe hemorrhagic fever with renal syndrome (HFRS). An extremely impaired IFN-γ-producing T cell response was observed in patients with severe HFRS at the early stage of infection, especially to the immunodominant epitopes detected in the mild to moderate group, namely peptides N127-141, N139-153, N241-255, and N355-369. The initially insufficient T cell response to the immunodominant epitopes may play a role in influencing the severity of HTNV infection. These findings provide information that may aid the design of future vaccines against hantaviruses.

Studies suggest that inflammation is involved in the colorectal cancer (CRC) pathology and symptoms. This study sought to quantitatively summarize the clinical cytokine data. Multiple reports have described the proportion of Th17 cells in peripheral blood and serum levels of Th17-related cytokines in patients with colorectal cancer (CRC). To clarify the status of Th17 cells and Th17-related cytokines in CRC patients, we did a meta-analysis of the results published previously to quantitatively assess the levels of peripheral Th17 cells and serum Th17-related cytokines in patients with CRC. We searched PubMed, Embase, web of Science, Cochrane Library and China National Knowledge Infrastructure (CNKI) systematically for studies reporting the proportion of Th17 cells and the serum levels of Th17-related cytokines (IL-17, IL-17A, IL-6, IL-22, IL-23) in CRC patients. Studies measuring the proportion of Th17 cells and the serum levels of Th17related cytokines (IL-17, IL-17A, IL-6, IL-22, IL-23) in CRC and healthy control subjects were included. Mean (standard deviation) proportion of Th17 cells and cytokine concentrations for CRC and control subjects were extracted. We assessed pooled data by using a random-effects model. We identified 1276 studies, of which 24 studies were included in the final meta-analytical processes. The quality was reliable according to the Newcastle-Ottawa Quality Assessment Scale (Case Control Studies). Compared with control subjects, CRC patients had a higher proportion of Th17 cells [2.37%, (0.53, 2.21)]; an elevated levels of serum IL-17A 1.11 pg./ml, 95%CI (0.16-2.07); an elevated levels of serum IL-6 3.42 pg/ml, 95%CI (3.14-3.70); an elevated levels of serum IL-22 1.32 pg/ml, 95%CI (0.94-1.70); an elevated levels of serum IL-23 0.16pg/ml, 95%CI(1.94-5.39). After sensitivity analysis, an elevated level of serum IL-17 was showed. The data showed that the proportion of Th17 cells in PB and levels of serum IL-17, IL-17A, IL-6, IL-22, IL-23 increased among CRC patients compared to control subjects. This result demonstrated that Th17 cells and Th17-related cytokines may be involved in the pathogenic mechanisms of CRC.