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Updated: Feb 2, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MicroRNA-382 inhibits cell growth and migration in colorectal cancer by targeting SP1
Yupeng Ren1, Hao Zhang2, Peng Jiang2
1Department of Colorectal Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, NO.44 Xiaoheyan Road, Dadong District, Shenyang, 110042, People's Republic of China. renyupeng_md@163.com.
Background:
Emerging evidence showed that microRNAs (miRs) play critical roles in human cancers by functioning as either tumor suppressor or oncogene. MIR-382 was found to function as tumor suppressor in certain cancers. However, the role of MIR-382 in colorectal cancer (CRC) is largely unknown. Specificity protein 1 (SP1) is highly expressed in several cancers including CRC and is correlated with poor prognosis, but it is unclear whether or not MIR-382 can regulate the expression of SP1.
Methods:
MIR-382 expression level was measured by reverse transcription-quantitative polymerase chain reaction. The connection between MIR-382 and SP1 was validated by luciferase activity reporter assay and western blot assay. Cell counting kit-8 assay and wound-healing assay were conducted to investigate the biological functions of MIR-382 in CRC.
Results:
In this study, we found MIR-382 expression was downregulated in CRC tissues and cell lines, and the transfection of MIR-382 mimic decreased cell growth and migration. Furthermore, we identified SP1 was a direct target of MIR-382. Overexpression of MIR-382 decreased the expression of SP1, whereas MIR-382 knockdown promoted SP1 expression. We also observed an inversely correlation between MIR-382 and SP1 in CRC tissues. Additionally, we showed that knockdown of SP1 inhibited cell growth and migration and attenuated the effect of MIR-382 inhibitor on cell behaviors.
Conclusions:
In conclusion, the present study describes a potential mechanism underlying a MIR-382/SP1 link contributing to CRC development. Thus, MIR-382 may be able to be developed as a novel treatment target for CRC.
Insights
MicroRNA-382 (MIR-382) acts as a tumor suppressor in colorectal cancer (CRC) by downregulating Specificity protein 1 (SP1). This MIR-382/SP1 interaction offers a potential new therapeutic target for CRC treatment.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- MicroRNAs (miRs) are crucial regulators in cancer, acting as tumor suppressors or oncogenes.
- MIR-382 is a known tumor suppressor in some cancers, but its role in colorectal cancer (CRC) remains unclear.
- Specificity protein 1 (SP1) is overexpressed in CRC and linked to poor prognosis, with its regulation by MIR-382 uninvestigated.
Purpose of the Study:
- To investigate the role of MIR-382 in colorectal cancer (CRC).
- To determine if MIR-382 regulates the expression of Specificity protein 1 (SP1) in CRC.
- To elucidate the functional consequences of the MIR-382/SP1 interaction in CRC development.
Main Methods:
- Quantitative polymerase chain reaction (qPCR) to measure MIR-382 expression.
- Luciferase reporter assays and Western blotting to validate the MIR-382 and SP1 interaction.
- Cell counting kit-8 and wound-healing assays to assess cell proliferation and migration.
Main Results:
- MIR-382 expression was significantly downregulated in CRC tissues and cell lines.
- MIR-382 overexpression inhibited CRC cell growth and migration, while its knockdown promoted these behaviors.
- SP1 was identified as a direct target of MIR-382; MIR-382 overexpression reduced SP1 levels, and knockdown increased them.
- An inverse correlation between MIR-382 and SP1 was observed in CRC tissues.
- SP1 knockdown mimicked the tumor-suppressive effects of MIR-382 and attenuated the impact of MIR-382 inhibition.
Conclusions:
- A novel MIR-382/SP1 regulatory axis was identified in colorectal cancer.
- This axis plays a significant role in CRC progression, suggesting MIR-382's tumor-suppressive function.
- MIR-382 represents a promising therapeutic target for colorectal cancer treatment.
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