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BACKGROUND The study was conducted to investigate the short-term complications and prognostic factors in patients with esophagogastric junction adenocarcinoma (EGJA). METHODS This retrospective study included 110 EGJA patients who underwent surgery from January 2010 to November 2012 at The First Affiliated Hospital of BengBu Medical College. The overall survival and short-term complications were analyzed according to the patients' clinical characteristics. RESULTS The incidence of postoperative cardiopulmonary complications was significantly higher in patients with preoperative cardiopulmonary disease or elderly patients (P < 0.05). Four cases of upper margin cancer residue were detected using the abdominal approach and three using the thoracic approach, which indicated that the cancer residue margin was related to surgical approach. The overall five-year survival rate was 34.3% and statistically differed according to pathological stage and en block resection (Pall < 0.05). Cox regression analysis showed that lymph node metastasis (P < 0.05) and the extent of tumor invasion (P < 0.05) were independent prognostic factors. CONCLUSION Elderly patients with preoperative cardiopulmonary disease had an increased risk of developing postoperative cardiopulmonary complications. Lymph node status and depth of tumor invasion were independent factors related to patient prognosis.

Triple negative breast cancer lacking estrogen receptor (ER), progesterone receptor and Her2 account for account for the majority of the breast cancer deaths, due to the lack of specific gene targeted therapy. Our current study aimed to investigate the role of miR-544 in triple negative breast cancer. Endogenous levels of miR-544 were significantly lower in breast cancer cell lines than in human breast non-tumorigenic and mammary epithelial cell lines. We found that miR-544 directly targeted the 3′-untranslated region (UTR) on both Bcl6 and Stat3 mRNAs, and overexpression of miR-544 in triple negative breast cancer cells significantly down-regulated expressions of Bcl6 and Stat3, which in turn severely inhibited cancer cell proliferation, migration and invasion in vitro. Employing a mouse xenograft model to examine the in vivo function of miR-544, we found that expression of miR-544 significantly repressed the growth of xenograft tumors. Our current study reported miR-544 as a tumor-suppressor microRNA particularly in triple negative breast cancer. Our data supported the role of miR-544 as a potential biomarker in developing gene targeted therapies in the clinical treatment of triple negative breast cancer.

Flavonoids from Astragalus complanatus R.Br (FAC) had anticancer effects on many tumor cells. The current study was performed to evaluate the effects of FAC on human breast cell proliferation, apoptosis, and metastasis, as well as their active mechanism. Cell viability and growth were detected using the cell counting kit (CCK)-8 assay in vitro. Assay of FAC on induced breast cancer mortality was counted as survival time of nude mice after breast cell line inoculation. The effect of FAC on cell invasion was investigated by an optimization assay that contains a 96-well Boyden chamber with wells precoated with BME at three different concentrations. The mechanism of its action on apoptosis and metastasis was determined by related gene detection. Proliferation of three breast cell lines was inhibited with FAC treatment in a dose-dependent manner. Survival time of nude mice with breast cancer cell inoculation also was prolonged with increasing FAC dose. Metastasis in FAC-treated breast cells was also significantly inhibited. Real-time polymerase chain reaction (PCR) assay demonstrated that apoptosis-related BCL-2 and caspase-9 gene expression was consistent with their phenotype change. Metastasis-related FAK and BRCA1 gene expression was inversely related to FAC treatment. Western blot analysis indicated that BCL-2 and FAK proteins were reduced, whereas caspase-9 and BRCA1 proteins were increased with a higher dose of FAC treatment. These data suggested that FAC has an important role in breast cancer growth and metastasis suppression in vitro and in vivo. Its active mechanism involves promoting programmed cancer cell death and regulates metastasis-related gene expression.

The small (SK3) and intermediate (IK1) conductance calcium-activated potassium channels could have key roles in the endothelium-dependent hyperpolarization factor pathway, which is believed to contribute to normal penile erection function. We aimed to investigate the expression of SK3 and IK1 in diabetic rodents. The experimental diabetes model was induced in 8-week-old male Sprague–Dawley rats (250–300 g) by a single administration of streptozotocin. Both the diabetes mellitus group (DM group, n = 20) and the control group (NDM group, n = 10) were injected with a low dose of apomorphine to allow for the measurement and comparison of the corresponding penile erections. The mRNA and protein expression levels of SK3 and IK1 were measured by reverse transcription polymerase chain reaction and western blot, respectively. Erectile function was significantly decreased in the DM group compared with control group (P < 0.05). The mRNA and protein expression levels of SK3 and IK1 were reduced in the cavernous tissue of diabetic rats compared with the control group (P < 0.05). Diabetes inhibits mRNA and protein expression of both SK3 and IK1 in the cavernous tissue of diabetic rats. This could play a key role in the development of erectile dysfunction in diabetic rats.

Colorectal cancer (CRC) causes significant mortalities worldwide. Fibroblast growth factor (FGF) receptor (FGFR) signaling is frequently dysregulated and/or constitutively activated in CRCs, contributing to cancer carcinogenesis and progression. Here, we studied the activity of AZD-4547, a novel and potent FGFR kinase inhibitor, on CRC cells. AZD-4547 inhibited CRC cell growth in vitro, and its activity correlated with the FGFR-1/2 expression level. AZD-4547 was cytotoxic and pro-apoptotic in FGFR-1/2-expressed CRC cell lines (NCI-H716 and HCT-116), but not in FGFR-1/2 null HT-29 cells. Further, AZD-4547 inhibited cell cycle progression and attenuated the activation of FGFR1-FGFR substrate 2 (FRS-2), ERK/mitogen-activated protein kinase (MAPK), and AKT/mammalian target of rapamycin (AKT/mTOR) signalings in NCI-H716 and HCT-116 cells. In vivo, AZD-4547 oral administration at effective doses inhibited NCI-H716 (high FGFR-1/2 expression) xenograft growth in nude mice. Phosphorylation of FGFR-1, AKT, and ERK1/2 in xenograft specimens was also inhibited by AZD-4547 administration. Thus, our preclinical studies strongly support possible clinical investigations of AZD-4547 for the treatment of CRCs harboring deregulated FGFR signalings.

The effect of Mg2+, NaCl and citric acid on the accumulation of β-carotene inDunaliella Salina was studied. The experimental results showed that 10.5 mmol/L Mg2+, 5 mol/L NaCl, 3 μmol/L citric acid, and CO2 are favorable forDunaliella Salina cell growth and β-carotene accumulation. After 144 h culture under the above conditions, theDunaliella Salina biomass increased by 7.18 times; β-carotene reached 9.61%.

PurposeIn a previous study, we found a hyaluronidase 3 (HYAL3) gene mutation in exon 2 at position 188 by genome sequencing in a lung squamous cell carcinoma patient. The mutation results in substitution of serine for alanine. The aim of the study was to screen the HYAL3 gene mutation in Chinese lung squamous cell carcinoma patients and explore the correlation between mutation of HYAL3 with clinical and pathological characteristics in lung squamous cell carcinoma patients in China.MethodsWe applied polymerase chain reaction to examine the HYAL3 gene mutations in cancer tissues and their adjacent normal tissues from 39 cases of lung squamous cell carcinoma patients.Results1) The incidence rate of HYAL3 mutation in 39 cases of lung squamous cell carcinoma was 10.26% (4/39) and none in adjacent normal lung tissues (0/39). 2) The mutations of HYAL3 in the 4 cases were all heterozygous: 3 of them were located in exon 1 (G-T) and one in exon 2 (G-T). 3) Mutations of the HYAL3 gene were not correlated with the distribution of patient gender, age, tumor size, histological grade, smoking history, TNM stage or distant metastasis ( P >0.05). The gene mutation was correlated with lymph node status ( P = 0.044).ConclusionMutations of the HYAL3 gene are rare in Chinese lung squamous cell carcinoma patients and might contribute to lymph node metastasis.

SK3, one of the small conductance calcium-activated potassium channels, is the key substance of the endothelium-derived hyperpolarizing factor (EDHF) passway. This study aimed to investigate the expression of SK3 in the cavernous tissue of rats with diabetes mellitus (DM).Twenty-six DM models were made by injection of streptozocin (STZ) out of 50 male Sprague-Dawley rats, and another 15 that failed to be modeled were included in an STZ group. Ten healthy male rats were taken as blank controls. Eight weeks later, the penile erectile function of the rats was detected by injection of apomorphine (APO) at 80 microg/kg, and the expression of SK3 in the cavernous tissue was determined by RT-PCR and Western blot.Penile erection was observed in 14 (54%) of the 26 DM rat models and in all the rats of the STZ and blank control groups. Both the mRNA and protein expressions of SK3 were significantly lower in the DM (0.50 +/- 0.09 and 0.65 +/- 0.06) than in the STZ (1.15 +/- 0.03 and 1.28 +/- 0.04) and blank control groups (1.21 +/- 0.04 and 1.34 +/- 0.05) (P0.05). There were no significant differences between the STZ and blank control groups in either penile erection or mRNA and protein expressions of SK3 (P0.05).Diabetes mellitus can significantly reduce erectile function in rats, which may be related to the decreased expression of SK3 in the corpus cavernosum.

Our aim was to investigate the mechanisms of early protection by ischemic preconditioning (IPC) of transplanted rat kidneys.Thirty-six male donor and recipient Sprague-Dawley (SD) rats were randomly divided into 3 groups: sham-operated (A), transplantation (B), and IPC treatment (C) groups. Group A underwent exploratory laparotomy, group B received orthotopic transplantation, and group C, 15 minutes of ischemia followed by 10 minutes of reperfusion before transplantation. We measured the serum creatinine (SCr), blood urea nitrogen (BUN), and degree of kidney graft ischemic/reperfusion injury (IRI) by tumor necrosis factor-alpha (TNF-alpha) IkappaB kinase beta (IKK-beta) nuclear factor-kappa beta (NF-kappabeta) p65 subunit mRNA expressions.The SCr and BUN levels in groups C and B were higher than those in the sham-operated group (P.01), without a significant difference between groups C and B at 24 hours after transplantation (P.05). The degree of renal graft tubular injury in group C was significantly lower than that in group B (P.01). TNF-alpha transcription levels at 24 hours after transplantation were significantly lower compared with the non-IPC group (P.01). However, we failed to note a significant difference in IKK-beta or p65 mRNA expressions between groups C and B (P.05).One cycle of preconditioning (15 min/10 min) attenuated renal graft IRI in the early phase. The inhibiting effects on TNF-alpha and the positive feedback signaling of TNF-alpha/NF-KB pathways may play important roles in renal graft protection.