L Cheng

The University of Hong Kong, Hong Kong, Hong Kong

Are you L Cheng?

Claim your profile

Publications (6)15.21 Total impact

  • Source
    Cell Death & Disease 08/2013; 4(8):e765. DOI:10.1038/cddis.2013.292 · 5.18 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: MicroRNAs are endogenous, non-coding RNAs of approximately 20-22 nucleotides that regulate genes expression by binding to the 3' untranslated region (UTR) of targets mRNAs and play critical roles in cancer pathways. Malignant glioma is the most common and highly lethal central nervous system tumor for which little effective treatment is available over several decades. The purpose of this study was to explore the therapeutic potential of plasmid-based microRNA-7 (miR-7) for gliomas in vivo. Enhancing miR-7 levels in vitro could significantly induce cell apoptosis, and inhibit cell proliferation, cell migration and invasion. Western blotting analysis was performed, which indicated that miR-7 directly inhibited epidermal growth factor receptor (EGFR) and further antagonized the downstream protein kinases including ERK, Akt and Stat3. Furthermore, systemic administration of miR-7 encapsulated in cationic liposome resulted in glioma xenografts growth arrest and the metastatic nodules decrease effectively in a sequence-specific manner. In this study, miR-7 was applied in glioma treatment for the first time in vivo. Our findings suggested that the plasmid-mediated gene therapy with miR-7 appeared to be a promising candidate for the development of new antitumor and anti-metastasis treatment for human glioma. Keywords: miR-7, glioma, metastasis, apoptosis, gene therapy.
    Neoplasma 02/2013; 60(03). DOI:10.4149/neo_2013_036 · 1.64 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Transfection of plasmid vectors coexpressing short hairpin RNA (shRNA) for focal adhesion kinase (FAK) and epidermal growth factor receptor (EGFR) significantly inhibited protein level of FAK and EGFR. Knockdown of FAK and EGFR expression significantly inhibited cell proliferation and induced cell apoptosis of A549 lung cancer cells in vitro. In A549 subcutaneous xenograft model, mice treated for 3 weeks with plasmid that coexpresses FAK and EGFR shRNA had significantly smaller tumors than those in control mice (P<0.01). FAK and EGFR dual silencing also significantly decreased microvessel density, tumor cell proliferation and increased the level of apoptosis in tumor cells. Moreover, administration with plasmid that coexpresses FAK and EGFR shRNA significantly inhibited the A549 experimental lung metastases. Collectively, our data suggest that the dual inhibition of FAK and EGFR by using plasmid vector-based RNA interference might be a novel therapeutic approach to the treatment of human NSCLC.Cancer Gene Therapy advance online publication, 18 January 2013; doi:10.1038/cgt.2012.91.
    Cancer gene therapy 01/2013; DOI:10.1038/cgt.2012.91 · 2.55 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Commonly used drugs for the treatment of colon{} cancer patients like CPT-11 shows severe side effects or induces resistance in clinical settings. Thus, we analyzed a combination of PLK1 (polo-like kinase 1)-specific short hair RNA (shRNA), a potent tool to destroy mitosis in cancer cells, together with CPT-11 to enhance drug sensitivity. Cellular proliferation and apoptosis were determined in SW620 colorectal carcinoma cells. Knockdown of cellular PLK1 led to the decreased mRNA and PLK1 protein in RT-PCR and western blot assay. The viability declined (pnohistochemistry, accompanied with TUNEL assay. As we expect, the combination treatment delayed tumor growth (p of PLK1-specific shRNA interference with low-dose CPT-11 triggered a antitumor efficacy and represented a potential strategy to treat colon cancer. Keywords: CPT-11, drug resistance, SN-38, PLK1, RNA interference, colorectal carcinoma.
    Neoplasma 08/2012; 59(6):676-84. DOI:10.4149/neo_2012_086 · 1.64 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Interleukin-15 (IL15) is a potential immunotherapeutic treatment for cancer. Caspy2 is an active zebra caspase for inducing apoptosis and immune response in murine tumors. In this study, we aim to evaluate the potential of gene therapy using IL15 and Caspy2 against the murine tumors. Plasmid expressing both Caspy2 and IL15 genes was constructed, encapsulated in DOTAP/cholesterol cationic liposome and injected intratumorally into the mice bearing CT26, B16-F10 and 4T1 carcinoma. We found that coexpression of IL15 and Caspy2 could significant inhibit tumor growth and prolong survival of the mice bearing CT26 or B16F10 tumor. A significant reduction in spontaneous lung metastasis was observed in the 4T1 tumor model. In CT26 model, the mice treated with IL15 and Caspy2 acquired a long-time protective immunity against the parental tumor cell rechallenge. Cytotoxic T lymphocytes and terminal deoxynucleotidyltransferase-mediated nick end labelling assays showed that the combination of capsy2 and IL15 could enhance both the apoptosis and immune response induction, which may account for its extraordinary antitumor effect. Furthermore, we showed that the observed tumor suppression by IL15 and Caspy2 concurred with the Caspy2-mediated downregulation of IL10 and upregulation of interferon-γ and tumor necrosis factor-α. Our results therefore suggested that the combination regimen might be a novel and effective strategy for cancer treatment.
    Cancer gene therapy 04/2012; 19(7):460-7. DOI:10.1038/cgt.2012.17 · 2.55 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Signal transducer and activator of transcription 3 (STAT3) plays an important role in the tumor formation and metastasis. In this study, short hairpin RNA targeting STAT3 was cloned into pGenesil-2 plasmid vector and the effects of STAT3 silencing in 4T1 breast cancer cells were analyzed both in vitro and in vivo. Forty-eight hours after transfecting with pSi-STAT3, the expression level of STAT3, the upstream regulator and downstream targets were measured using Western blot. Moreover, the effects of pSi-STAT3 on migration and invasion in 4T1 cells were tested using wound-healing and tube formation assay. Furthermore, 4T1 subcutaneous mice model was used to evaluate the effects of pSi-STAT3 on tumor growth and metastasis. Proliferation, apoptosis, angiogenesis in tumor tissues and lung metastases were measured by PCNA, TUNEL, and CD31 immunostaining, respectively. Our results indicated that siRNA targeting STAT3 could significantly silence STAT3 expression in 4T1 breast cancer cells and result in inhibition of 4T1 breast cells migration and HUVECs tube formation. In vivo, pSi-STAT3 delayed tumor growth (pknockdown of STAT3 by plasmid-based siRNA might be a potential therapy against breast cancer.
    Neoplasma 01/2011; 58(6):538-47. DOI:10.4149/neo_2011_06_538 · 1.64 Impact Factor

Publication Stats

18 Citations
15.21 Total Impact Points


  • 2013
    • The University of Hong Kong
      Hong Kong, Hong Kong
  • 2012–2013
    • Sichuan University
      • State Key Laboratory of Biotherapy
      Hua-yang, Sichuan, China