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1.
Mol Med Rep ; 23(2)2021 02.
Article in English | MEDLINE | ID: mdl-33300085

ABSTRACT

The development of chemotherapeutic dug resistance hinders the clinical treatment of cancer. MicroRNAs (miRNAs/miRs) have been revealed to serve essential roles in the drug resistance of numerous types of cancer. miR­139­5p was previously reported to be associated with cisplatin (DDP) sensitivity in human nasopharyngeal carcinoma cells and colorectal cancer cells. However, the effect and underlying mechanism of miR­139­5p in DDP sensitivity in non­small cell lung cancer (NSCLC) cells has not yet been fully elucidated. In the present study, the expression of miR­139­5p and Homeobox protein Hox­B2 (HOXB2) in NSCLC tissues was examined by reverse transcription­quantitative polymerase chain reaction (RT­qPCR) and western blotting. Subsequently, the effect of miR­139­5p on the DDP sensitivity of NSCLC cells in vitro was investigated. Cell proliferation was examined using a Cell Counting Kit­8 assay. Western blotting was used to evaluate the protein expression of HOXB2, phosphorylated (p)­PI3K, p­AKT, caspase­3 and cleaved­caspase­3, and RT­qPCR was used to evaluate the expression of miR­139­5p, and the mRNA expression levels of HOXB2, PI3K, AKT and caspase­3. The apoptotic rate of the cells was detected using flow cytometry. miR­139­5p expression in NSCLC tissues was shown to be significantly lower compared with that in adjacent tissues. Additionally, miR­139­5p increased cell apoptosis and inhibited NSCLC cell proliferation induced by DDP in vitro via modulating the PI3K/AKT/caspase­3 signaling pathway. Furthermore, HOXB2 was identified to be a target of miR­139­5p, and miR­139­5p was revealed to sensitize NSCLC cells to DDP via the targeting of HOXB2. Taken together, the results of the present study demonstrated that regulating the expression of miR­139­5p could provide a novel approach to reverse DDP resistance and increase chemosensitivity in the treatment of NSCLC.


Subject(s)
Apoptosis/drug effects , Carcinoma, Non-Small-Cell Lung/metabolism , Cell Proliferation/drug effects , Cisplatin/pharmacology , Homeodomain Proteins/metabolism , Lung Neoplasms/metabolism , MicroRNAs/metabolism , Neoplasm Proteins/metabolism , RNA, Neoplasm/metabolism , Transcription Factors/metabolism , A549 Cells , Aged , Carcinoma, Non-Small-Cell Lung/drug therapy , Carcinoma, Non-Small-Cell Lung/genetics , Carcinoma, Non-Small-Cell Lung/pathology , Female , Homeodomain Proteins/genetics , Humans , Lung Neoplasms/drug therapy , Lung Neoplasms/genetics , Lung Neoplasms/pathology , Male , MicroRNAs/genetics , Middle Aged , Neoplasm Proteins/genetics , RNA, Neoplasm/genetics , Transcription Factors/genetics
2.
Front Microbiol ; 10: 2211, 2019.
Article in English | MEDLINE | ID: mdl-31681182

ABSTRACT

Antimicrobial peptides (AMPs) represent the largest group of endogenous compounds and serves as a novel alternative to traditional antibiotics for the treatment of pathogenic microorganisms. Moricin is an important α-helical AMP plays a crucial role in insect humoral defense reactions. The present study was designed to identify and characterize novel AMP moricin (Px-Mor) from diamondback moth (Plutella xylostella) and tested its activity against bacterial and fungal infection including the opportunistic human pathogen Aureobasidium pullulans. Molecular cloning of Px-Mor using rapid amplification of cDNA ends revealed a 482 bp full length cDNA with 198 bp coding region. The deduced protein sequence contained 65 amino acids, and the mature peptides contained 42 amino acid residues with a molecular mass of 4.393 kDa. Expression analysis revealed that Px-Mor was expressed throughout the life cycle of P. xylostella with the highest level detectable in the fourth instar and prepupa stage. Tissue specific distribution showed that Px-Mor was highly expressed in fat body and hemocyte. In vitro, antimicrobial assays indicated that Px-Mor exhibited a broad antimicrobial spectrum against Gram positive bacteria (GPB), Gram negative bacteria (GNB) and fungi. Moreover, scanning electron microscopy and transmission electron microscopy (TEM) revealed that Px-Mor can cause obvious morphological alterations in A. pullulans, which demonstrated its powerful effect on the mycelia growth inhibition. Taken together, these results indicate that Px-Mor plays an important role in the immune responses of P. xylostella and can be further exploited as an antimicrobial agent against various diseases including for the treatment of A. pullulans infection.

3.
J Cancer Res Ther ; 11 Suppl 2: C173-8, 2015 Oct.
Article in English | MEDLINE | ID: mdl-26506871

ABSTRACT

PURPOSE: To evaluate the efficacy and oncologic outcomes of transoral laser microsurgery (TLM) for recurrent laryngeal carcinoma after previous treatment. MATERIALS AND METHODS: A systematic search in PubMed was performed using mesh word for "laryngeal cancer," crossed with "recurrent," and "TLM." The primary endpoints, including overall survival (OS) rate, local control rate, and disease-specific survival (DSS) were summarized using RevMan software. Adverse events and complications were recorded if reported. RESULTS: The pooled odds ratios (ORs) for main outcomes, including local control, 5-year OS, and DSS were 3.08 (95% confidential indexed [95% CI], 1.88-5.05), 2.29 (95% CI, 1.42-3.67), and 5.05 (95% CI, 2.75-9.27), respectively. The pooled OR for functional outcome, larynx preservation, was 3.82 (95% CI, 2.46-5.94), whereas the pooled risk difference of local recurrence was 45% (95% CI, 26-64%). CONCLUSIONS: It seems that TLM is an effective option for recurrent laryngeal cancer with regard to the high incidence of OS, local control, and especially organ preservation. However, more prospective studies are needed to confirm its efficiency.


Subject(s)
Laryngeal Neoplasms/pathology , Laryngeal Neoplasms/surgery , Microsurgery/methods , Humans , Laryngeal Neoplasms/mortality , Laryngeal Neoplasms/therapy , Microsurgery/adverse effects , Neoplasm Recurrence, Local , Odds Ratio , Postoperative Complications , Retreatment , Treatment Outcome
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