MiR-103a-3p Promotes Tumorigenesis of Breast Cancer by Targeting ETNK1.

Background: We aimed to elucidate the molecular mechanism of miR-103a-3p regulating breast cancer progression. Methods: Firstly, clinical tissues was obtained from 2019-2023 at Yancheng Third People's Hospital, Yancheng, China. miR-103a-3p or ETNK1 expression in clinical tissues or breast cancer cell lines was analyzed with qRTPCR. MDA-MB-231 cells were performed with miR-103a-3p inhibitor or mimic, and OE-ETNK1. The proliferation and apoptosis ability were detected by CCK-8 and TUNEL assay. The xenograft models were established by inoculating transfected MDA-MB-231 cells to BALB/c mice. Results: miR-103a-3p showed an overexpression and was related to poor prognosis in breast cancer. miR-103a-3p-deprived MDA-MB-231 cells displayed weaker levels of cell proliferation and higher rates of apoptosis. In contrast, ETNK1 was downregulated in breast cancer and proved to be a downstream target of miR-103a-3p. Xenograft models subjected to either miR-103a-3p antagomir treatment or ETNK1-knockdown resulted in tumor growth suppression. Conclusion: miR-103a-3p might promote breast cancer progression by inhibiting ETNK1.

Total mesorectal excision plus lateral lymph node dissection vs TME on rectal cancer patients: a meta-analysis.

OBJECTIVE: Our study is the first meta-analysis to compare total mesorectal excision (TME) plus lateral lymph node dissection (LLND) with TME on rectal cancer patients regarding outcomes including overall survival, disease-free survival, local recurrence, complications, urinary dysfunction, and sexual dysfunction. METHODS: PubMed, Embase, and Cochrane library were searched for publications up to October 2019. Two investigators independently screened the studies for eligibility and extracted specific data. Relevant data were analyzed by Review Manager version 5.3. RESULTS: Patients in TME + LLND group suffered more complications (OR = 1.48, 95% CI [1.07, 2.03], P = 0.02) compared with TME group; no significant difference was observed in overall survival (HR = 1.11, 95% CI [0.77, 1.61], P = 0.57), disease-free survival (HR = 1.05, 95% CI [0.85, 1.30], P = 0.64), local recurrence (OR = 0.93, 95% CI [0.56, 1.54], P = 0.78), and urinary dysfunction (OR = 1.60, 95% CI [0.66, 3.87], P = 0.3). CONCLUSION: TME + LLND may cause more complications compared with TME on rectal cancer patients. However, the definite conclusion still requires more researches.

MicroRNA-4513 Promotes Gastric Cancer Cell Proliferation and Epithelial-Mesenchymal Transition Through Targeting KAT6B.

The purpose of this study was to investigate the expression level of microRNA-4513 (miR-4513) in gastric cancer (GC), and to elucidate the mechanisms underlying its regulation of GC progression. Quantitative real-time PCR (qRT-PCR) was performed to measure the expression level of miR-4513 in GC cells. Transfection efficacy of synthetic miRNAs was examined by qRT-PCR. After synthetic miRNA transfection, cell counting kit-8 assay and transwell invasion assay were conducted to measure biological changes in these groups. The key molecular expression level involved in epithelial-mesenchymal transition (EMT) was analyzed by Western blot. Bioinformatic analysis and Western blot were performed to investigate the connection between miR-4513 and lysine acetyltransferase 6B (KAT6B). qRT-PCR results showed that miR-4513 expression level was upregulated in GC cell lines. Downregulation of miR-4513 expression inhibited GC cell proliferation, invasion, and EMT. KAT6B was validated as a direct target of miR-4513. In addition, KAT6B expression level can be upregulated by miR-4513 inhibitor. Collectively, we showed that miR-4513 is involved in regulating the biological function of GC cells via KAT6B. In addition, miR-4513 may serve as a potential target for the molecular therapy of GC.

Evaluation of the Treatment Process of Landfill Leachate Using the Toxicity Assessment Method.

Landfill leachate is composed of a complex composition with strong biological toxicity. The combined treatment process of coagulation and sedimentation, anaerobics, electrolysis, and aerobics was set up to treat landfill leachate. This paper explores the effect of different operational parameters of coagulation and sedimentation tanks and electrolytic cells, while investigating the combined process for the removal efficiency of physicochemical indices after processing the landfill leachate. Meanwhile, a battery of toxicity tests with Vibrio fischeri, zebrafish larvae, and embryos were conducted to evaluate acute toxicity and calculated the toxicity reduction efficiency after each treatment process. The combined treatment process resulted in a 100% removal efficiency of Cu, Cd and Zn, and a 93.50% and an 87.44% removal efficiency of Ni and Cr, respectively. The overall removal efficiency of chemical oxygen demand (COD), ammonium nitrogen (NH4⁺-N), and total nitrogen (TN) were 93.57%, 97.46% and 73.60%, respectively. In addition, toxicity test results showed that the acute toxicity of landfill leachate had also been reduced significantly: toxicity units (TU) decreased from 84.75 to 12.00 for zebrafish larvae, from 82.64 to 10.55 for zebrafish embryos, and from 3.41 to 0.63 for Vibrio fischeri. The combined treatment process was proved to be an efficient treatment method to remove heavy metals, COD, NH4⁺-N, and acute bio-toxicity of landfill leachate.

Decreased expression and prognostic role of EHD2 in human breast carcinoma: correlation with E-cadherin.

Decreased expression of epithelial cadherin (E-cadherin) has been noted to associate with aggressiveness and metastasis of breast cancer. The aim of this study was to examine the effect of C-Terminal EH domain-containing protein 2 (EHD2) expression on E-cadherin and related mechanism in the metastasis of breast cancer. Immunohistochemical analysis was performed in 96 human breast carcinoma samples and the data were correlated with clinicopathologic characteristics. Furthermore, Western blot analysis was performed for EHD2 and E-cadherin in breast carcinoma samples and cell lines to evaluate their protein levels and molecular interaction. We found that the expression of EHD2 was positively related with E-cadherin expression (P < 0.01), moreover, EHD2 expression was significantly correlated with histologic grade (P < 0.01). Meanwhile, E-cadherin expression obtained similar results. Kaplan-Meier survival analysis showed that decreased expression of EHD2 and E-cadherin exhibited a significant correlation with poor prognosis in human breast cancer (P < 0.01). While in vitro, we employed siRNA technique to knock down EHD2 expressions and observed their effects on breast cancer cells growth. EHD2 depletion by siRNA promoted PCNA expression, and it was concurrent with the decreased expression of epithelial marker E-cadherin and the increased expression of N-cadherin by Western blot analysis. Consistent with these observations, the suppression of EHD2 in breast cancer cells remarkably promoted cellular proliferation and migration. On the basis of these results, we suggested that EHD2 can inhibit the metastasis of human breast cancer by regulating the EMT key markers E-cadherin and N-cadherin.