HCP5 promotes colon cancer development by activating AP1G1 via PI3K/AKT pathway.

OBJECTIVE: To explore whether HCP5 participates in the pathogenic progression of colon cancer (CC) and its underlying mechanism. PATIENTS AND METHODS: HCP5 expression in CC tissues and cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between the HCP5 expression and tumor stage of CC patients was then analyzed. After CC cells were transfected with HCP5-siRNA, the proliferation and migration capacities were detected by cell counting kit-8 (CCK-8), colony formation and transwell assay, respectively. Cell cycle was examined by flow cytometry. Western blot was conducted to detect protein expressions of HCP5, AP1G1 and relative molecules in the PI3K/AKT pathway. Rescue experiments were performed by co-transfection of HCP5-siRNA and AP1G1-siRNA into CC cells, followed by cell function detection. RESULTS: HCP5 was highly expressed, whereas AP1G1 was lowly expressed in CC tissues and cell lines. Besides, CC patients with stage III-IV presented higher expression of HCP5 than those with stage I-II. The knockdown of HCP5 in CC cells down-regulated proliferation and migration capacities, and arrested cell cycle in the G0/G1 phase, which was reversed by the AP1G1 knockdown. In addition, HCP5 knockdown up-regulated AP1G1 expression, whereas down-regulated the expression of relative proteins in the PI3K/AKT pathway. CONCLUSIONS: HCP5 was significantly increased in CC and enhanced the proliferation and migration of CC cells by inhibiting the AP1G1 expression. HCP5 promoted CC development by activating the PI3K/AKT pathway.

A systematic review of the evidence base for vidian neurectomy in managing rhinitis.

BACKGROUND: Vidian neurectomy has been proposed as a surgical option for rhinitis refractory to medical treatment. However, the evidence base for its benefit remains controversial. METHODS: A systematic review was performed. Studies reporting original data on patients with rhinitis treated by vidian neurectomy were included. Patient-reported outcome measures were the primary outcome investigated; specific peri-operative morbidities were the secondary outcome. RESULTS: A total of 1012 articles fulfilled the search criteria, 32 of which were included in the study. Patient-reported outcome measures were compared before and after surgery in eight studies. There were 529 patients represented in these trials. Significant improvement in rhinorrhoea was reported in all eight studies. Temporary dry eyes was reported in 24.63 per cent of cases (272 out of 1104 cases). There was no report of cranial nerve deficit or eye movement disturbance. CONCLUSION: Endoscopic vidian neurectomy does have a role in the surgical management of refractory rhinitis, particularly in patients with non-allergic rhinitis, but a well-designed cohort trial would be advantageous to clarify long-term outcomes.

Melatonin prevents gentamicin-induced testicular toxicity and oxidative stress in rats.

This study investigated the protective effects of melatonin (MT) against gentamicin (GM)-induced testicular toxicity and oxidative damage in rats. GM (100 mg kg(-1) ) was injected intraperitoneally (i.p.) to rats for 6 days. MT (15 mg kg(-1) ) was administered i.p. to rats for 6 days at 1 hr after the GM treatment. GM caused a decrease in prostate and seminal vesicle weights, sperm count and sperm motility. Histopathological examination showed various morphological alterations in the testis, characterised by degeneration of spermatogonia/spermatocytes, decrease in the number of early spermatogenic cells and vacuolisation. In addition, an increased malondialdehyde concentration and decreased glutathione content and glutathione reductase, catalase and glutathione-S-transferase activities were found in the testis. In contrast, MT treatment significantly attenuated the testicular toxicity of GM, including decreased reproductive organ weights, sperm count, and sperm motility and increased histopathological alterations. MT also had an antioxidant benefit by decreasing the lipid peroxidative product malondialdehyde and increasing the level of the antioxidant glutathione and the activities of antioxidant enzymes in the testis. These results indicate that MT prevents testicular toxicity induced by GM in rats, presumably due to its potent antioxidant activity, and its ability to inhibit lipid peroxidation, and restore antioxidant enzyme activity.

Apoptotic cell death in rat epididymis following epichlorohydrin treatment.

Epichlorohydrin (ECH) is an antifertility agent that acts both as an epididymal toxicant and an agent capable of directly affecting sperm motility. This study identified the time course of apoptotic cell death in rat epididymides after ECH treatment. Rats were administrated with a single oral dose of ECH (50 mg/kg). ECH-induced apoptotic changes were evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and its related mechanism was confirmed by Western blot analysis and colorimetric assay. The TUNEL assay showed that the number of apoptotic cells increased at 8 h, reached a maximum level at 12 h, and then decreased progressively. The Western blot analysis demonstrated no significant changes in proapoptotic Bcl-2-associated X (Bax) and anti-apoptotic Bcl-2 expression during the time course of the study. However, phospho-p38 mitogen-activated protein kinase (p-p38 MAPK) and phospho-c-Jun amino-terminal kinase (p-JNK) expression increased at 8-24 h. Caspase-3 and caspase-8 activities also increased at 8-48 h and 12-48 h, respectively, in the same manner as p-p38 MAPK and p-JNK expression. These results indicate that ECH induced apoptotic changes in rat epididymides and that the apoptotic cell death may be related more to the MAPK pathway than to the mitochondrial pathway.