Related Experiment Video
Updated: Aug 14, 2026

Murine Model for Non-invasive Imaging to Detect and Monitor Ovarian Cancer Recurrence
Published on: November 2, 2014
[Experimental therapy of survivin antisense oligonucleotide for human ovarian cancer cell SKOV3]
Shu-Qin Wei1, Sheng Bi, Jian-Hua Zheng
1Department of Obstetrics & Gynecology, The First Clinical College, Harbin Medical University, Harbin, Heilongjiang, 150001, PR China. weishuqin@hotmail.com
Background & Objective:
Survivin abnormally overexpresses in a variety of human tumors, it may play an important role in the development of tumor. This study was designed to investigate the inhibitory effects of survivin antisense oligonucleotide (ASODN) on human ovarian carcinoma cell SKOV3 in vivo and its mechanism.
Methods:
SKOV3 cells were transfected with survivin ASODN mediated by DOTAP liposome reagent, MTT method was used to observe the inhibitory rate, Western blot analysis was used to determine relating gene expression. Flow cytometry, DNA ladder analysis, and DAPI staining were used to examine cell apoptosis. Kinase activity test was used to examine the changes of caspase-3 activity.
Results:
The expression of survivin in SKOV3 cells decreased after transfected with survivin ASODN. Survivin ASODN has obviously inhibited the growth of SKOV3 cells after transfection. The inhibitory rate of 1000 ng/ml ASODN transfection group was (60.30+/-2.95)%, which is obviously higher than control group (P< 0.05). Survivin ASODN transfection induced cell cycle arrest in G1 phrase, while the apoptotic rate increased from 0.65% to 32.10%. Caspase-3 activity (0.998+/-0.001) increased significantly after transfected with survivin ASODN (P< 0.01).
Conclusion:
Survivin ASODN,which can inhibit human ovarian carcinoma SKOV3 cells proliferation and induce apoptosis, is a prospective anti-cancer drug.
Insights
Survivin antisense oligonucleotide (ASODN) effectively inhibits human ovarian cancer cell growth by reducing survivin expression and inducing apoptosis. This suggests ASODN is a promising anti-cancer therapeutic for ovarian carcinoma.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Survivin is overexpressed in various human tumors, potentially driving tumor development.
- Targeting survivin offers a potential strategy for cancer therapy.
Purpose of the Study:
- To investigate the inhibitory effects of survivin antisense oligonucleotide (ASODN) on human ovarian carcinoma SKOV3 cells.
- To elucidate the mechanism of ASODN-mediated inhibition in ovarian cancer.
Main Methods:
- SKOV3 cells were transfected with survivin ASODN using DOTAP liposomes.
- Cell proliferation was assessed by MTT assay; gene expression by Western blot.
- Apoptosis was analyzed using flow cytometry, DNA laddering, and DAPI staining; caspase-3 activity was measured.
Main Results:
- Survivin expression was significantly reduced in SKOV3 cells post-ASODN transfection.
- ASODN transfection inhibited SKOV3 cell proliferation, with a 1000 ng/ml dose yielding a 60.30% inhibition rate.
- ASODN induced G1 cell cycle arrest, increased apoptosis from 0.65% to 32.10%, and significantly elevated caspase-3 activity.
Conclusions:
- Survivin ASODN effectively inhibits human ovarian carcinoma SKOV3 cell proliferation.
- ASODN induces apoptosis in ovarian cancer cells, indicating a potential anti-cancer mechanism.
- Survivin ASODN represents a prospective therapeutic agent for ovarian cancer treatment.
Related Concept Videos
Cancer Therapies
However, cancer treatments can pose several challenges, as therapies used to kill cancer cells are generally also toxic to normal cells. Moreover, cancer cells mutate rapidly and can develop resistance to chemical agents or radiation therapy. Besides, all types of cancer cells may not respond to the same therapy. Some cancer cells respond to one...
Targeted Cancer Therapies
There are several types of targeted therapies against specific...
Treatment Resistant Cancers
Targeted Cancer Therapies
There are several types of targeted therapies against specific...
Treatment Resistent Cancers

