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Updated: Oct 21, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
LncRNA-PANDAR regulates the progression of thyroid carcinoma by targeting miR-637/KLK4
Yi Qing1, Qian Li2, Ling-Yan Zhao3
1Department of Oncology, Affiliated Hospital of Chengdu University, Chengdu 610081, People's Republic of China.
Abstract:
Thyroid gland carcinoma (TC) originates from follicular or parafollicular thyroid cells and is one of the most common endocrine organ malignancies. To explore the molecular mechanism by which long-chain non-coding RNAs regulate the growth and metastasis of thyroid gland carcinoma, in this study we focused on long non-coding RNAs (lncRNAs) that have been reported to be involved in tumorigenesis. We identified Promoter Region of CDKN 1A antisense DNA damage-activated RNA (PANDAR), which was positively correlated with thyroid gland carcinoma risk. PANDAR could promote thyroid gland carcinoma cell proliferation and metastasis. PANDAR negatively correlated with miR-637, and miR-637 overexpression suppressed thyroid gland carcinoma progression, which could be reversed by PANDAR. MiR-637 could target Kallikrein-related peptidases 4 (KLK4) to inhibit its expression, which was high in thyroid gland carcinoma. KLK4 inhibited cell progression in thyroid gland carcinoma cells. Knockdown of PANDAR expression inhibited cancer progression in nude mice. Overall, PANDAR can suppress miR-637 and induce KLK4 to regulate invasion and migration in thyroid gland carcinoma. Additionally, we identified miR-637 as a target of PANDAR in thyroid gland carcinoma, and PANDAR can be used as a novel therapeutic target for the treatment of thyroid gland carcinoma.
Insights
Promoter Region of CDKN 1A antisense DNA damage-activated RNA (PANDAR) promotes thyroid cancer growth and metastasis by suppressing miR-637 and upregulating KLK4. PANDAR represents a potential therapeutic target for thyroid gland carcinoma.
Area of Science:
- Molecular Oncology
- RNA Biology
- Endocrinology
Background:
- Thyroid gland carcinoma (TC) is a common endocrine malignancy.
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in tumorigenesis.
- Understanding lncRNA regulation in TC is crucial for developing new therapies.
Purpose of the Study:
- To investigate the molecular mechanisms of lncRNAs in thyroid gland carcinoma progression.
- To identify specific lncRNAs involved in TC growth and metastasis.
- To explore PANDAR as a potential therapeutic target in TC.
Main Methods:
- Identification and analysis of lncRNAs in thyroid gland carcinoma.
- Investigating the correlation between PANDAR, miR-637, and KLK4 expression.
- Functional assays to assess the impact of PANDAR and miR-637 on TC cells.
- In vivo studies using nude mice to evaluate PANDAR's role in cancer progression.
Main Results:
- PANDAR expression is positively correlated with thyroid gland carcinoma risk.
- PANDAR promotes TC cell proliferation and metastasis by suppressing miR-637.
- miR-637 targets KLK4, and its suppression by PANDAR leads to increased KLK4 expression.
- KLK4 inhibits cell progression in TC.
- Knockdown of PANDAR inhibited tumor growth in vivo.
Conclusions:
- PANDAR promotes thyroid gland carcinoma invasion and migration by suppressing miR-637 and inducing KLK4.
- miR-637 acts as a tumor suppressor in TC.
- PANDAR is a novel therapeutic target for thyroid gland carcinoma treatment.
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