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Updated: Mar 21, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
microRNA-141 inhibits thyroid cancer cell growth and metastasis by targeting insulin receptor substrate 2
Su Dong1, Xianying Meng2, Shuai Xue2
1Department of Anesthesia, The First Hospital of Jilin University 71# Xinmin Street, Chaoyang District, Changchun, Jilin 130021, P. R. China.
Abstract:
microRNA-141 (miR-141), a member of the miR-200 family, and has been reported to involve in tumor initiation and development in many types of cancers. However, the function and underlying molecular mechanism of miR-141 in thyroid cancer remains unclear. Therefore, the aim of this study is to identify its expression, function, and molecular mechanism in thyroid cancer. In this study, we found that miR-141 expression levels were downregulated in human thyroid cancer specimens compared to the adjacent normal tissues, and its expression were strongly correlated with clinical stages and lymph node metastases. Function assays showed that overexpression of miR-141 inhibited cell proliferation, induced cell apoptosis, and decreased migration, invasion in thyroid cancer cells, as well as tumor growth in nude mice. Moreover, insulin receptor substrate 2 (IRS2), a known oncogene, was confirmed as a direct target of miR-141, and IRS2 expression levels were upregulated in thyroid cancer, and its expression were inversely correlated with miR-141 expression levels in human thyroid cancer specimens. Forced expression of IRS2 reversed the inhibition effect induced by miR-141 overexpression in thyroid cancer cells. Taken together, our study provides the first evidence that miR-141 suppressed thyroid cancer cell growth and metastasis through inhibition of IRS2. Thus, miR-141 might serve as a promising therapeutic strategy for thyroid cancer treatment.
Insights
microRNA-141 (miR-141) is downregulated in thyroid cancer, inhibiting tumor growth and metastasis by targeting the oncogene insulin receptor substrate 2 (IRS2). This suggests miR-141 as a potential therapeutic strategy for thyroid cancer.
Area of Science:
- Molecular Oncology
- Cancer Biology
- Biochemistry
Background:
- microRNA-141 (miR-141), part of the miR-200 family, is implicated in various cancers.
- The specific role and mechanism of miR-141 in thyroid cancer pathogenesis are not well understood.
Purpose of the Study:
- To investigate the expression, function, and molecular mechanism of miR-141 in thyroid cancer.
- To determine if miR-141 can be a therapeutic target for thyroid cancer.
Main Methods:
- Analysis of miR-141 expression in thyroid cancer tissues versus normal tissues.
- In vitro functional assays (proliferation, apoptosis, migration, invasion) in thyroid cancer cells.
- In vivo tumor growth assays in nude mice.
- Identification and validation of miR-141 targets using molecular biology techniques.
Main Results:
- miR-141 expression is significantly downregulated in thyroid cancer and correlates with advanced clinical stage and lymph node metastasis.
- Overexpression of miR-141 suppresses thyroid cancer cell proliferation, induces apoptosis, and reduces migration and invasion.
- Insulin receptor substrate 2 (IRS2) is identified as a direct target of miR-141, with its expression inversely correlated with miR-141 levels in tumors.
- Restoration of IRS2 expression abrogates the inhibitory effects of miR-141.
Conclusions:
- miR-141 acts as a tumor suppressor in thyroid cancer.
- miR-141 inhibits thyroid cancer cell growth and metastasis by downregulating IRS2.
- miR-141 represents a potential novel therapeutic agent for thyroid cancer treatment.
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