We have located links that may give you full text access.
COMPARATIVE STUDY
JOURNAL ARTICLE
Reduced high-mobility group box 1 expression induced by RNA interference inhibits the bioactivity of hepatocellular carcinoma cell line HCCLM3.
Digestive Diseases and Sciences 2012 January
BACKGROUND: Increased expression of high-mobility group box 1 (HMGB1) has been observed in many tumor types, but the role of HMGB1 in hepatocellular carcinoma (HCC) is unknown.
AIMS: To examine the effects of RNA interference HMGB1 on the bioactivity of HCC cell line HCCLM3.
METHODS: We synthesized three specific small interfering RNAs of HMGB1 (HMGB1-siRNAs) and transfected these into HCCLM3 cells by use of Lipofectamine 2000. RT-PCR and Western blot were performed to determine the effects of HMGB1-siRNAs on HMGB1 expression and to detect NF-κB/p65 and VEGF-C expression after transfection of HMGB1-siRNAs into HCCLM3. In vitro proliferation was assessed by MTT assay. Migration and invasive ability were determined by use of the Transwell assay. Apoptosis was demonstrated by flow cytometry.
RESULTS: RT-PCR and Western blotting showed that all three specific HMGB1-siRNAs significantly inhibited HMGB1 expression, with inhibition by HMGB1-siRNA-1 being highest (70-80%). MTT assay demonstrated that the growth of cells transfected with HMGB1-siRNA-1 was significantly lower than that of control cells (P < 0.01). The Transwell assay showed that cell migration and invasion were significantly inhibited in HMGB1 knockdown cells compared with control cells (P < 0.01). FCM revealed that apoptosis was significantly increased in HMGB1-siRNA-1-transfected cells compared with control cells (P < 0.01). Expression of NF-κB/p65 and VEGF-C was inhibited in HCCLM3 cells transfected with HMGB1-siRNA-1 compared with control cells (P < 0.01).
CONCLUSION: Downregulation of HMGB1 could obviously inhibit the growth of HCCLM3 cells, and their migration and invasion ability. HMGB1 may serve as a potential target for treatment of HCC.
AIMS: To examine the effects of RNA interference HMGB1 on the bioactivity of HCC cell line HCCLM3.
METHODS: We synthesized three specific small interfering RNAs of HMGB1 (HMGB1-siRNAs) and transfected these into HCCLM3 cells by use of Lipofectamine 2000. RT-PCR and Western blot were performed to determine the effects of HMGB1-siRNAs on HMGB1 expression and to detect NF-κB/p65 and VEGF-C expression after transfection of HMGB1-siRNAs into HCCLM3. In vitro proliferation was assessed by MTT assay. Migration and invasive ability were determined by use of the Transwell assay. Apoptosis was demonstrated by flow cytometry.
RESULTS: RT-PCR and Western blotting showed that all three specific HMGB1-siRNAs significantly inhibited HMGB1 expression, with inhibition by HMGB1-siRNA-1 being highest (70-80%). MTT assay demonstrated that the growth of cells transfected with HMGB1-siRNA-1 was significantly lower than that of control cells (P < 0.01). The Transwell assay showed that cell migration and invasion were significantly inhibited in HMGB1 knockdown cells compared with control cells (P < 0.01). FCM revealed that apoptosis was significantly increased in HMGB1-siRNA-1-transfected cells compared with control cells (P < 0.01). Expression of NF-κB/p65 and VEGF-C was inhibited in HCCLM3 cells transfected with HMGB1-siRNA-1 compared with control cells (P < 0.01).
CONCLUSION: Downregulation of HMGB1 could obviously inhibit the growth of HCCLM3 cells, and their migration and invasion ability. HMGB1 may serve as a potential target for treatment of HCC.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app