Publications by authors named "Lujun Dai"

3 Publications

  • Page 1 of 1

Serum exosomal microRNAs as predictive markers for EGFR mutations in non-small-cell lung cancer.

J Clin Lab Anal 2021 May 8;35(5):e23743. Epub 2021 Mar 8.

Department of Infectious Diseases, Affiliated Hangzhou First people's Hospital, Zhejiang University School of Medicine, Hangzhou, China.

Background: Current therapeutic drugs show positive effects on non-small-cell lung cancer (NSCLC) patients with mutant epidermal growth factor receptor (EGFR) expression, whereas a lesser beneficial effect is generally noted on NSCLC patients with wild-type EGFR. Therefore, identification of new detection methods for the accurate clinical diagnosis of NSCLC is essential.

Methods: In this study, tumor-derived exosomes from the plasma of EGFR mutation and wild-type NSCLC patients were isolated. Extensive exosomal miRNA profiling of EGFR mutation and wild-type NSCLC patients, in comparison with healthy individuals, was performed using miRNA-sequencing analysis.

Results: The variation of exosomal miRNA expression between control group (NR) and NCSLC samples (AM and AW) was identified. 96 significantly different expressed miRNAs were identified. Of these, 39 miRNAs were upregulated and 57 were downregulated. 11 miRNAs were downregulated, and 31 miRNAs were upregulated in the miRNA expression between NR and AM. Compared with healthy donors, 54 upregulated miRNAs and 36 downregulated miRNAs were observed in samples from AW patients. 40 different expressed miRNAs were identified in AM samples, compared with AW. Ten of upregulated miRNAs are miR-260, miR-1169, miR-117, miR-15b-5p, miRNA-731, miR-342-5p, miR- 898, miR-1384, miR-56, and miR-1214. Ten of downregulated miRNAs are miR-99b-5p, miR-1116, miR-689, miR-818, miR-604, miR-72, miR-955, miR-403, miR-1228, and miR-836.

Conclusion: The exosomal miR-1169 and miR-260 as potential candidates, which contain specific characteristics that can distinguish between wild-type EGFR and mutant EGFR NSCLC patients in early-stage cancers.
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http://dx.doi.org/10.1002/jcla.23743DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8128312PMC
May 2021

Ganoderic acid DM induces autophagic apoptosis in non-small cell lung cancer cells by inhibiting the PI3K/Akt/mTOR activity.

Chem Biol Interact 2020 Jan 23;316:108932. Epub 2019 Dec 23.

Department of Infectious Diseases, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, 310006, Hangzhou, Zhejiang, China. Electronic address:

The incidence and mortality of lung cancer are the highest among cancer-related deaths. However, the long-term use of currently available cytotoxic drugs can increase genetic alterations in cancer cells and cause drug-resistance, which significantly limits their usage. Since current systemic treatment options are limited, effective chemotherapeutic agents are urgently needed for non-small cell lung cancer (NSCLC) treatment. In this study, we demonstrated that ganoderic acid DM (GA-DM) could increase apoptosis in A549 and NCI-H460 NSCLC cells. GA-DM treatment decreased the protein expression levels of Bcl-2 and increased the expression levels of Bax, cleaved caspase-3 and cleaved PRAP. Furthermore, GA-DM could promote autophagic flux, and the cytotoxic effect against cancer cells of GA-DM was significantly inhibited by targeted suppression of autophagy, suggesting that autophagy contributed to GA-DM-induced cell death in NSCLC. Moreover, GA-DM clearly induced autophagy by inactivating the PI3K/Akt/mTOR pathway. When overexpression of Akt reactivated Akt/mTOR pathway in A549 or NCI-H460 cells, the increase of autophagy related marker LC3B-II and apoptosis related protein cleaved PARP and cleaved caspase 3 and the ration of apoptotic cells by GA-DM was reversed, suggesting that GA-DM promoted autophagy and apoptosis by inhibiting Akt/mTOR pathway-mediated autophagy induction. In conclusion, our study indicated that GA-DM can induce autophagic apoptosis in NSCLC by inhibiting Akt/mTOR activity. (209 words).
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http://dx.doi.org/10.1016/j.cbi.2019.108932DOI Listing
January 2020

Relationship of SOCS3 and TGF-β with IDO expression in early pregnancy chorionic villi and decidua.

Exp Ther Med 2017 Nov 19;14(5):4817-4824. Epub 2017 Sep 19.

Department of Pathology, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China.

We aimed to investigate the expression of suppressors cytokine signaling (SOCS)-3, transforming growth factor (TGF)-β and indoleamine 2,3-dioxygense (IDO) and to analyse the relationship of SOCS3 and TGF-β with IDO expression in early pregnancy chorionic villi and decidua in the maternal-fetal interface. Western blot analysis and immunohistochemical method were used to detect the expression of TGF-β, SOCS3 and IDO in chorionic villi and decidua tissues of normal pregnant women. SOCS3, TGF-β and IDO protein was identified in chorionic villi and decidua tissues of normal pregnant women and there was a negative correlation between the expression of IDO and SOCS3, but TGF-β expression was positively correlated with IDO expression. The levels of IDO expression in the decidua from normal pregnancies were significantly higher than those in chorionic villi, while the expression of SOCS3 was no significant difference between decidua and chorionic villi. In normal physiological state of pregnancy, SOCS3 and TGF-β may be involved in the regulation of immune tolerance by positive or negative regulation of IDO expression at maternal fetal interface.
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http://dx.doi.org/10.3892/etm.2017.5142DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5704277PMC
November 2017
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