Related Experiment Video
Updated: Mar 2, 2026

Dextran Enhances the Lentiviral Transduction Efficiency of Murine and Human Primary NK Cells
Published on: January 15, 2018
The Effects of Lentivirus-mediated shRNA Interference Targeting Mcl-1 on Growth of NK/T-cell Lymphoma
Abstract:
Myeloid leukemia-1 (Mcl-1) gene has been reported as an important factor in various types of cancer, but little research was processed on natural killer (NK)/T-cell lymphoma, a kind of a highly aggressive disease with a poor prognosis. Here we investigated the expression of Mcl-1 in seven lymphoma cell lines and its potential role as a molecular drug target for NK/T-cell lymphoma therapy by using lentivirus-mediated shRNA interference targeting Mcl-1 (lenti-shMcl-1). In our study, the expression of Mcl-1 in different lymphoma cell lines were evaluated firstly, after that lenti-shMcl-1 was constructed and transduced into NK/T-cell lymphoma cell line SNK-6 which had a high level expression of Mcl-1. Methylthiazolete-Trazolium (MTT) assay and flow cytometry (FCA) were employed to detect the status of proliferation and apoptosis after infection. Lastly we investigated the effects of chemotherapy agent vincristine (VCR) combination with lenti-shMcl-1 by MTT and FCA assay. The results showed that Mcl-1 gene expressed in all seven lymphoma cell lines at different levels. Recombinant lentiviruses could infect SNK-6 cells effectively. Mcl-1 expression level was remarkably down-regulated after infection with lenti-shMcl-1. The growth of SNK-6 cells was inhibited significantly through apoptosis pathway. Otherwise, lenti-shMcl-1 also revealed a significant chemosensitizing effect in combination with vincristine. In a word, we demonstrated that lenti-shMcl-1 had a significant anti-NK/T cell lymphoma effect and targeting Mcl-1 therapy could be a promising novel approach in treatment of lymphoma.
Insights
Targeting the Myeloid leukemia-1 (Mcl-1) gene with lentivirus-mediated shRNA interference (lenti-shMcl-1) effectively inhibited natural killer (NK)/T-cell lymphoma cell growth. This approach also enhanced chemotherapy sensitivity, showing promise for lymphoma treatment.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- Myeloid leukemia-1 (Mcl-1) is implicated in various cancers.
- Its role in natural killer (NK)/T-cell lymphoma, an aggressive disease, is under-investigated.
- NK/T-cell lymphoma has a poor prognosis, necessitating novel therapeutic strategies.
Purpose of the Study:
- To investigate Mcl-1 expression in lymphoma cell lines.
- To evaluate the therapeutic potential of targeting Mcl-1 in NK/T-cell lymphoma.
- To assess the efficacy of lentivirus-mediated shRNA interference targeting Mcl-1 (lenti-shMcl-1).
Main Methods:
- Expression analysis of Mcl-1 across seven lymphoma cell lines.
- Construction and transduction of lenti-shMcl-1 into SNK-6 cells.
- Methylthiazolete-Trazolium (MTT) and flow cytometry (FCA) assays to assess proliferation and apoptosis.
- Combination therapy evaluation with vincristine (VCR).
Main Results:
- Mcl-1 was expressed in all tested lymphoma cell lines.
- Lenti-shMcl-1 effectively transduced and down-regulated Mcl-1 expression in SNK-6 cells.
- Targeting Mcl-1 significantly inhibited SNK-6 cell proliferation via apoptosis.
- Lenti-shMcl-1 demonstrated a synergistic chemosensitizing effect with vincristine.
Conclusions:
- Mcl-1 is a relevant target in NK/T-cell lymphoma.
- Lenti-shMcl-1 exhibits significant anti-lymphoma activity.
- Targeting Mcl-1 represents a promising novel therapeutic approach for lymphoma treatment.

