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As for postoperative comorbidities, there were significant differences in intraperitoneal hemorrhage and pleural effusion between the elderly group and the non-elderly group. Moreover, the median follow-up time was 38.5 months, and the overall survival of elderly patients with comorbidities was significantly lower than that of the elderly patients without comorbidities (p<0.05).

LAG can be performed safely and successfully in the elderly population with acceptable postoperative and long-term results.

LAG can be performed safely and successfully in the elderly population with acceptable postoperative and long-term results.

To investigate the expression of miR-614 in serum of gastric cancer patients and its effect on invasion and proliferation of gastric cancer cell line HGC-27.

Thirty patients with gastric cancer from May 2016 to November 2018 comprised the research group, and 30 healthy people undergoing physical examination in the same period comprised the control group. The expression of miR-614 in tissues and miR-614 in HGC-27 cell line was detected by qRT-PCR, miR-614-mimics was transfected into HGC-27, while miR-614-mimics group, blank control group and negative control group were established respectively. Cell invasion was detected by Transwell method, and CCK-8 method was used to detect the effect of miR-614 transfection on the proliferation of HGC-27 cells on the 1st, 2nd, 3rd and 4th day.

The expression of miR-614 in the research group was significantly lower than in the control group (p<0.05). The number of cells passing through the invasion microvessel membrane in miR-614-mimics group was significantly lower than in negative control group and blank control group (p<0.05) 24 h after transfection. On the 3rd and 4th day, the cell proliferation of miR-614-mimics group was significantly lower than in blank group and negative control group (p<0.05).

In conclusion, miR-614 is lowly expressed in gastric cancer patients and inhibits the invasion and proliferation of gastric cancer cell line HGC-27.

In conclusion, miR-614 is lowly expressed in gastric cancer patients and inhibits the invasion and proliferation of gastric cancer cell line HGC-27.

Considering that cyclin D1 had a prognostic and clinical value for breast cancer patients, adequate measurement of cyclin D1 is necessary.

In this investigation, we detect cyclin D1 expression in tumour and peritumoral tissue of breast cancer patients by Western blotting method and by immunohistochemistry.

Cyclin D1 expression decreased significantly with each advanced clinical stage of disease and tumour size. Also, patients without lymph node involvement, with positive hormone receptors and Luminal A type of tumours had significantly increased the expression of cyclin D1. We show that cyclin D1 expression correlates with longer RFS in the entire group of patients, in the group of ER-positive and in the group of HER2-negative patients. Patients who were both ER and cyclin D1 positive had a better prognosis.

Taken together, our results, showing correlation of cyclin D1 with clinical stage, tumour size and lymph nodes, suggest that cyclin D1 expression, detected by Western blotting, could be considered as an additional marker for the staging of breast cancer, as well as a marker for longer RFS and survival in ER-positive breast cancer patients.

Taken together, our results, showing correlation of cyclin D1 with clinical stage, tumour size and lymph nodes, suggest that cyclin D1 expression, detected by Western blotting, could be considered as an additional marker for the staging of breast cancer, as well as a marker for longer RFS and survival in ER-positive breast cancer patients.

The purpose of this study was to evaluate Ki67 as a biomarker for response to concurrent chemo-radiotherapy in previously treated patients with standard chemotherapy protocols in the neoadjuvant setting (NACT).

Evaluated were 33 patients treated concurrently with radiotherapy and capecitabine. All patients had residual disease after anthracycline-docetaxel based NACT, verified with imaging techniques and clinical exams. Response rate (RR) was evaluated 3 months after completion of the concurrent treatment, and was correlated to tumor immune-histochemical characteristics. Binary logical regression was used for model testing and correlation of Ki67 and RR. An Omnibus test showed the model to be statistically significant and that a set of depending variables can be used as predictors for treatment response with p=0.021. Model -2 log likelihood with Nagelkerke R Square were used to define significance of other tumor characteristics besides Ki67.

Only Ki67 showed statistically significant correlation with RR, as high Ki67 predicts that there will be no response to concurrent capecitabine - radiotherapy treatment in chemo-resistant advanced breast cancer. Other characteristics such as histological grade, estrogen or progesterone receptors, HER2 overexpression or lymphovascular or perineural invasion showed no significance.

High value of Ki67 is a negative predictor for response in concurrent capecitabine-radiotherapy treatment in chemo-resistant advanced breast cancer.

High value of Ki67 is a negative predictor for response in concurrent capecitabine-radiotherapy treatment in chemo-resistant advanced breast cancer.

This study aimed to explore the role of MIR31HG and its molecular mechanism in breast cancer (BC).

The levels of MIR31HG in BC tissues and cell lines were detected. The correlations of MIR31HG expression level with clinical characteristics and prognosis of patients were analyzed. Then we detected the effects of MIR31HG on the proliferative, migrative and invasive abilities of BC cells. Subsequently, we detected the level of the predicted target POLDIP2 in BC. Furthermore, the effect of POLDIP2 on the malignant phenotype of MIR31HG-mediated BC was evaluated through recovery experiments.

MIR31HG was aberrantly up-regulated in BC tissues and cell lines, and its level was in correlation with the patient's tumor diameter, tumor node metastasis (TNM) stage, lymph node metastasis as well as the overall survival rate. Besides, MIR31HG knockdown was able to inhibit the proliferative ability, migration and invasion of BC cells. Besides, POLDIP2 was aberrantly up-regulated in BC tissues, and its expression level was in positive correlation with the level of MIR31HG. Besides, POLDIP2 overexpression could partially inhibit the proliferative, migrative and invasive abilities of BC cells. Long non-coding (lnc)RNA MIR31HG was aberrantly up-regulated in BC and its expression was associated with poor prognosis of BC patients. Additionally, the levels of MIR31HG and POLDIP2 were positively correlated.

The low expression of MIR31HG or POLDIP2 can inhibit the proliferative, migrative and invasive abilities of BC cells, which provides a new target for the diagnosis along with the treatment of BC.

The low expression of MIR31HG or POLDIP2 can inhibit the proliferative, migrative and invasive abilities of BC cells, which provides a new target for the diagnosis along with the treatment of BC.

The view that microRNA-224 (miR-224) may lead to tumorigenesis has been accepted in many studies. However, its role remains unclear in modulating the chemosensitivity of breast cancer cells to docetaxel (DOC). Thus, the aim of this study was to estimate what's the role of miR-224 in the chemosensitivity of breast cancer cells to DOC.

The role of miR-224 in breast cancer cells was analyzed using CCK-8 assay, real-time PCR, flow cytometry assay and Western blot. Dual-luciferase reporter assay and API-5-siRNA technology were performed to analyze the association between miR-224 and Apoptosis inhibitor 5 (API-5).

Overexpression of miR-224 could significantly decrease the chemosensitivity of MCF-7 breast cancer cells to DOC. The luciferase activity of MCF-7/DOC cells containing wild-type 3'UTR of API-5 could be inhibited by miR-224 mimics. Similarly, the chemoresistance of MCF-7 cells to DOC induced by miR-224 mimics could be partially reversed by API-5-siRNA.

An inverse association between miR-224 and API-5 in breast cancer cells was revealed. Dysregulation of miR-224 plays a vital role in the acquired DOC resistance of breast cancer and at least partially via targeting API-5.

An inverse association between miR-224 and API-5 in breast cancer cells was revealed. Dysregulation of miR-224 plays a vital role in the acquired DOC resistance of breast cancer and at least partially via targeting API-5.

We aimed to uncover the role of METTL3 in stimulating the stemness and progression of breast cancer (BCa) through mediating N6-methyladenosine (m6A) modification on SOX2 mRNA.

METTL3 levels in 48 paired BCa and adjacent normal ones were examined. Kaplan-Meier method was introduced for assessing the prognostic value of METTL3 in BCa. Liraglutide Regulatory effects of METTL3 on invasive and migratory abilities in MCF-7 cells were evaluated by Transwell assay. Besides, the protein levels of SOX2 and tumor stem cell markers CD133 and CD44 in MCF-7 cells affected by METTL3 were determined by Western blot. In addition, the potential interaction between METTL3 and SOX2 was ascertained through RIP (RNA-Binding Protein Immunoprecipitation) assay. Moreover, the interaction between IGF2BP2 and SOX2 influenced by METTL3 was verified by RIP assay as well.

METTL3 was upregulated in BCa tissues, especially in T3-T4 or those accompanied with lymphatic metastasis. BCa patients expressing a high level of METTL3 suffered worse prognosis. Knockdown of METTL3 downregulated protein levels of SOX2, CD133 and CD44 in MCF-7 cells. Moreover, invasive and migratory abilities were attenuated in BCa cells with METTL3 knockdown. Silencing of IGF2BP2 markedly downregulated SOX2. RIP assay confirmed the binding between METTL3 and SOX2 mRNA, and knockdown of METTL3 decreased the enrichment of SOX2 in anti-IGF2BP2. Interestingly, overexpression of SOX2 partially reversed the regulatory effects of downregulated METTL3 on MCF-7 cells.

METTL3 is upregulated in BCa, and it promotes the stemness and malignant progression of BCa through mediating m6A modification on SOX2 mRNA.

METTL3 is upregulated in BCa, and it promotes the stemness and malignant progression of BCa through mediating m6A modification on SOX2 mRNA.

The purpose was to investigate the effect of activated human hepatic stellate cell (HSC) microenvironment on the metastatic capacity of hepatocellular carcinoma (HCC) cells and its underlying mechanism.

LX-2 HSCs were stimulated with Human Transforming Growth Factor-Beta 1(TGF-β1), and protein expression of α-smooth muscle actin (α-SMA) and filamentous actin (F-actin) were determined to verify the activation of LX-2 cells. Next, SMMC7721 HCC cells were cultured in the conditioned medium originating from activated LX-2 cells. Wound healing and Transwell assays were performed to examine cell migration and invasion. The expression of metastasis-related genes Matrix Metalloproteinase9 (MMP9), N-cadherin, and Vascular endothelial growth factor (VEGF) was detected. ELISA was carried out to determine the interleukin (IL) -1β level. Finally the inhibitors of TGF-β1 and IL-1β were employed to investigate the roles of LX-2 activation and IL-1β in the metastasis-related gene alterations.

TGF-β1 activated LX-2 cells, as evidenced by up-regulated α-SMA and F-actin expression.