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Updated: Dec 30, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
The function of SNHG7/miR-449a/ACSL1 axis in thyroid cancer
Linchi Guo1,2, Jixuan Lu1,2, Jie Gao1,2
1Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Abstract:
Thyroid cancer (TC) has been characterized as the most common malignant malady of the endocrine system. Small nucleolar RNA host gene 7 (SNHG7) has been reported to serve as a key regulator in a large number of human cancer types, but its role in TC and the underlying regulatory mechanism have never been evaluated yet. The present study indicated that the expression of SNHG7 was markedly higher in TC cell lines. Knockdown of SNHG7 led to a suppression of TC cell progression and migration. Acyl-CoA synthetase long-chain family member 1 (ACSL1) has also been demonstrated as an oncogene in many cancers. Herein an inhibition of ACSL1 after SNHG7 knockdown was captured. Further, the suppressing effects of SNHG7 knockdown on TC cell processes were counteracted by ACSL1 overexpression. Data from online bioinformatics analysis, RNA immunoprecipitation, and luciferase reporter assays validated the interaction between microRNA-449a (miR-449a) and SNHG7 or ACSL1. It was also verified that SNHG7 sequestered miR-449a and therefore elevated ACSL1 expression levels. To conclude, the current study indicated that SNHG7 promoted proliferation and migration of TC cells by sponging miR-449a and therefore upregulating ACSL1. The present study may provide more explorations about the molecular regulation mechanism of long noncoding RNAs in TC progression.
Insights
Small nucleolar RNA host gene 7 (SNHG7) promotes thyroid cancer (TC) progression by sponging microRNA-449a (miR-449a) and upregulating Acyl-CoA synthetase long-chain family member 1 (ACSL1). This study elucidates a novel regulatory mechanism in TC development.
Area of Science:
- Endocrinology
- Molecular Biology
- Oncology
Background:
- Thyroid cancer (TC) is the most prevalent endocrine malignancy.
- The role and mechanism of Small nucleolar RNA host gene 7 (SNHG7) in TC remain unclear.
- Acyl-CoA synthetase long-chain family member 1 (ACSL1) is implicated as an oncogene in various cancers.
Purpose of the Study:
- To investigate the role of SNHG7 in thyroid cancer progression.
- To elucidate the underlying molecular mechanism involving microRNA-449a (miR-449a) and ACSL1.
- To explore SNHG7 as a potential therapeutic target in TC.
Main Methods:
- Quantitative real-time PCR to assess SNHG7 expression.
- SNHG7 knockdown and ACSL1 overexpression in TC cell lines.
- Bioinformatics analysis, RNA immunoprecipitation, and luciferase reporter assays to validate molecular interactions.
Main Results:
- SNHG7 expression is significantly upregulated in TC cell lines.
- SNHG7 knockdown suppresses TC cell proliferation and migration.
- SNHG7 acts as a molecular sponge for miR-449a, leading to increased ACSL1 expression, which promotes TC progression.
Conclusions:
- SNHG7 promotes thyroid cancer cell proliferation and migration via the SNHG7/miR-449a/ACSL1 axis.
- This finding reveals a novel regulatory pathway for long noncoding RNAs in TC.
- Targeting the SNHG7/miR-449a/ACSL1 pathway may offer a new therapeutic strategy for TC.
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