CRISPR/Cas9-mediated high-mobility group A2 knockout inhibits cell proliferation and invasion in papillary thyroid carcinoma cells

Jin, Shan; Yong, Hong; Liu, Yousheng; Bao, Wuyuntu

doi:10.1016/j.advms.2023.10.001

Cited by 2 publications

(3 citation statements)

References 27 publications

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“…Recent research has utilized CRISPR/Cas9 technology to knockout or knockdown various functional genes, aiding researchers in comprehending their cellular level functions across diverse metabolisms, pathways, and biological processes. Jin et al [17] used the CRISPR/Cas9 system to establish a HMGA2 knockout PTC cell line in order to exploring the HMGA2 effect on PTC cell proliferation and invasion. A Cluster of differentiation 16 α (CD16A) knockout human embryonic stem (hESC) cell line was constructed and was used to investigate the role of CD16A in the human cell development [18].…”

Section: Discussionmentioning

confidence: 99%

The Complement Component 4 Binding Protein α Gene: A Versatile Immune Gene That Influences Lipid Metabolism in Bovine Mammary Epithelial Cell Lines

Chen,

Zhao,

Jiang

et al. 2024

IJMS

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Complement component 4 binding protein α (C4BPA) is an immune gene which is responsible for the complement regulation function of C4BP by binding and inactivating the Complement component C4b (C4b) component of the classical Complement 3 (C3) invertase pathway. Our previous findings revealed that C4BPA was differentially expressed by comparing the transcriptome in high-fat and low-fat bovine mammary epithelial cell lines (BMECs) from Chinese Holstein dairy cows. In this study, a C4BPA gene knockout BMECs line model was constructed via using a CRISPR/Cas9 system to investigate the function of C4BPA in lipid metabolism. The results showed that levels of triglyceride (TG) were increased, while levels of cholesterol (CHOL) and free fatty acid (FFA) were decreased (p < 0.05) after knocking out C4BPA in BMECs. Additionally, most kinds of fatty acids were found to be mainly enriched in the pathway of the biosynthesis of unsaturated fatty acids, linoleic acid metabolism, fatty acid biosynthesis, and regulation of lipolysis in adipocyte. Meanwhile, the RNA-seq showed that most of the differentially expressed genes (DEGs) are related to PI3K-Akt signaling pathway. The expressions of 3-Hydroxy-3-Methylglutaryl-CoA Synthase 1 (HMGCS1), Carnitine Palmitoyltransferase 1A (CPT1A), Fatty Acid Desaturase 1 (FADS1), and Stearoyl-Coenzyme A desaturase 1 (SCD1) significantly changed when the C4BPA gene was knocked out. Collectively, C4BPA gene, which is an immune gene, played an important role in lipid metabolism in BMECs. These findings provide a new avenue for animal breeders: this gene, with multiple functions, should be reasonably utilized.

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Section: Discussionmentioning

confidence: 99%

The Complement Component 4 Binding Protein α Gene: A Versatile Immune Gene That Influences Lipid Metabolism in Bovine Mammary Epithelial Cell Lines

Chen,

Zhao,

Jiang

et al. 2024

IJMS

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“…The use of the CRISPR/Cas9 system for targeted gene therapy against tumors has been widely reported. In doxorubicin-resistant BC cells, flow cytometric analysis showed that targeting MDR1 using the CRISPR/Cas9 system increased drug accumulation within the cell compared with untreated cells ( 135 ). Song et al.…”

Section: Gene Therapy Methodsmentioning

confidence: 99%

“…In addition, in papillary thyroid carcinoma cells, the CRISPR/Cas9-mediated knockout of HMGA2 inhibited cell proliferation and invasion. It was suggested that HMGA2 knockout blocked the cell cycle in the G2/M phase and promoted cell necrosis ( 135 ). The results mentioned above showed that targeting HMGA2 using CRISPR/Cas9 technology can reduce drug resistance in cancers.…”

Section: Gene Therapy Methodsmentioning

confidence: 99%

HMGA2 promotes cancer metastasis by regulating epithelial–mesenchymal transition

Ma,

Ye,

Liu

et al. 2024

Front. Oncol.

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Epithelial–mesenchymal transition (EMT) is a complex physiological process that transforms polarized epithelial cells into moving mesenchymal cells. Dysfunction of EMT promotes the invasion and metastasis of cancer. The architectural transcription factor high mobility group AT-hook 2 (HMGA2) is highly overexpressed in various types of cancer (e.g., colorectal cancer, liver cancer, breast cancer, uterine leiomyomas) and significantly correlated with poor survival rates. Evidence indicated that HMGA2 overexpression markedly decreased the expression of epithelial marker E-cadherin (CDH1) and increased that of vimentin (VIM), Snail, N-cadherin (CDH2), and zinc finger E-box binding homeobox 1 (ZEB1) by targeting the transforming growth factor beta/SMAD (TGFβ/SMAD), mitogen-activated protein kinase (MAPK), and WNT/beta-catenin (WNT/β-catenin) signaling pathways. Furthermore, a new class of non-coding RNAs (miRNAs, circular RNAs, and long non-coding RNAs) plays an essential role in the process of HMGA2-induced metastasis and invasion of cancer by accelerating the EMT process. In this review, we discuss alterations in the expression of HMGA2 in various types of cancer. Furthermore, we highlight the role of HMGA2-induced EMT in promoting tumor growth, migration, and invasion. More importantly, we discuss extensively the mechanism through which HMGA2 regulates the EMT process and invasion in most cancers, including signaling pathways and the interacting RNA signaling axis. Thus, the elucidation of molecular mechanisms that underlie the effects of HMGA2 on cancer invasion and patient survival by mediating EMT may offer new therapeutic methods for preventing cancer progression.

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CRISPR/Cas9-mediated high-mobility group A2 knockout inhibits cell proliferation and invasion in papillary thyroid carcinoma cells

Cited by 2 publications

References 27 publications

The Complement Component 4 Binding Protein α Gene: A Versatile Immune Gene That Influences Lipid Metabolism in Bovine Mammary Epithelial Cell Lines

The Complement Component 4 Binding Protein α Gene: A Versatile Immune Gene That Influences Lipid Metabolism in Bovine Mammary Epithelial Cell Lines

HMGA2 promotes cancer metastasis by regulating epithelial–mesenchymal transition

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