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Updated: May 2, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
miR-101 inhibits cell proliferation by targeting Rac1 in papillary thyroid carcinoma
Xiaojie Lin1, Hongyu Guan1, Hai Li1
1Department of Endocrinology and Diabetes Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, P.R. China.
Abstract:
Accumulating evidence suggests that some microRNAs (miRNAs) are involved in papillary thyroid carcinoma (PTC) progression. However, it remains necessary to elucidate the underlying molecular mechanisms involved. In the present study, we investigated the role of microRNA-101 (miR-101) in PTC via targeting of Ras-related C3 botulinum toxin substrate 1 (Rac1). The results showed that miR-101 was significantly downregulated in PTC tissues compared with adjacent normal tissues. Restoration of miR-101 expression significantly inhibited cell proliferation in the K1 PTC cell line. Moreover, algorithm-based and experimental strategies verified Rac1 as a direct target of miR-101 in the K1 cell line. Taken together, these findings suggest that miR-101 inhibited PTC growth via the downregulation of Rac1 expression, providing a better understanding of miRNA-modulated signaling networks for future cancer therapeutics.
Insights
MicroRNA-101 (miR-101) is downregulated in papillary thyroid carcinoma (PTC). Restoring miR-101 inhibits PTC cell growth by targeting Ras-related C3 botulinum toxin substrate 1 (Rac1).
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) play a role in papillary thyroid carcinoma (PTC) progression.
- The specific molecular mechanisms underlying miRNA involvement in PTC require further elucidation.
Purpose of the Study:
- To investigate the role of microRNA-101 (miR-101) in PTC.
- To determine if miR-101 targets Ras-related C3 botulinum toxin substrate 1 (Rac1) in PTC.
Main Methods:
- Compared miR-101 expression in PTC tissues and adjacent normal tissues.
- Restored miR-101 expression in the K1 PTC cell line to assess effects on cell proliferation.
- Utilized computational algorithms and experimental validation to identify direct targets of miR-101.
Main Results:
- miR-101 was significantly downregulated in PTC tissues compared to normal tissues.
- Restoration of miR-101 expression inhibited proliferation of K1 PTC cells.
- Rac1 was confirmed as a direct molecular target of miR-101 in K1 cells.
Conclusions:
- miR-101 inhibits PTC growth by downregulating Rac1 expression.
- This study enhances understanding of miRNA-modulated signaling in PTC.
- Findings suggest potential therapeutic strategies targeting the miR-101/Rac1 axis in cancer treatment.
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