Effects of a Small Interfering RNA Targeting YKL-40 Gene on the Proliferation and Invasion of Endometrial Cancer HEC-1A Cells

Li, Lili; Fan, Jiangtao; Li, Dahai; Liu, Yan

doi:10.1097/igc.0000000000000774

Cited by 10 publications

(7 citation statements)

References 22 publications

(10 reference statements)

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“…Therefore, the HEC‐1A cell line was selected for subsequent studies. It was observed that small interfering RNA (siRNA) targeting YKL‐40 (si YKL‐40 ) could inhibit the proliferation, migration, and invasion of HEC‐1A cells (Li et al, 2016). It was also found that YKL‐40 was upregulated in EC and was correlated with the poor prognosis (Li et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Knockdown of YKL‐40 inhibits angiogenesis through regulation of VEGF/VEGFR2 and ERK1/2 signaling in endometrial cancer

Chen

Zhou

Luo

et al. 2021

Cell Biology International

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Studies have demonstrated that small interfering RNA (siRNA) targeting YKL‐40 (siYKL‐40) inhibits the proliferation, migration, invasion, and induces antiapoptotic abilities of endometrial cancer (EC) HEC‐1A cells. However, its effect on angiogenesis is unclear. The present study aimed to investigate the role of YKL‐40 in endometrial cancer and the related molecular mechanisms. YKL‐40 was knocked down by transfection with siYKL‐40 and the effects on angiogenesis, cell viability, and signaling pathways were investigated. The results showed that siYKL‐40 inhibited VEGFA levels and tube formation in endothelial cells. Additionally, inhibition of YKL‐40 decreased the expression levels of vascular endothelial growth factor (VEGF), phosphorylated vascular endothelial growth factor receptor 2 (pVEGFR2), and phosphorylated extracellular signal‐regulated kinases 1 and 2 (pERK1/2). Furthermore, a nude mice xenograft model of EC showed that siYKL‐40 inhibited tumor growth. Inhibition of YKL‐40 led to suppression of angiogenesis and reduction of microvessel density through VEGF/VEGFR2 and ERK1/2 signaling in endometrial cancer cells. Taken together, this study demonstrated novel molecular mechanisms for role of YKL‐40 in EC.

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Section: Introductionmentioning

confidence: 99%

Knockdown of YKL‐40 inhibits angiogenesis through regulation of VEGF/VEGFR2 and ERK1/2 signaling in endometrial cancer

Chen

Zhou

Luo

et al. 2021

Cell Biology International

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“…In gastric cancer, GATA6 has been shown to cooperate with other TFs, such as KLF5, to promote cancer development [ 34 , 35 ]. In CRC, GATA6 and Krüppel-like factor 5 (KLF5) have been implicated in the regulation of cancer stem cell characteristics and chemoresistance [ 36 , 37 ]. Signal transducer and activator of transcription 3 (STAT3) is a TF involved in various cellular processes, including cell growth, differentiation, and survival.…”

Section: Discussionmentioning

confidence: 99%

Unraveling molecular similarities between colorectal polyps and colorectal cancer: a systems biology approach

Radak,

Fallahi

2024

Intest Res

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Background/Aims: Colorectal cancer (CRC) and colorectal polyps are intimately linked, with polyps acting as precursors to CRC. Understanding the molecular mechanisms governing their development is crucial for advancing diagnosis and treatment. Employing a systems biology approach, we investigated the molecular similarities between polyp and CRC. Methods: We analyzed gene expression profiles, protein-protein interactions, transcription factors, and gene ontology to identify common differentially expressed genes (DEGs) and unravel shared molecular pathways. Results: Our analysis revealed 520 commonly dysregulated genes in polyps and CRC, serving as potential biomarkers and pivotal contributors to disease progression. Gene ontology analysis elucidated distinct biological processes associated with upregulated and downregulated DEGs in both conditions, highlighting common pathways, including signal transduction, cell adhesion, and positive regulation of cell proliferation. Moreover, protein-protein interaction networks shed light on subnetworks involved in rRNA processing, positive regulation of cell proliferation, mRNA splicing, and cell division. Transcription factor analysis identified major regulators and differentially expressed transcription factors in polyp and CRC. Notably, we identified common differentially expressed transcription factors, including ZNF217, NR3C1, KLF5, GATA6, and STAT3, with STAT3 and NR3C1 exhibiting increased expression. Conclusions: This comprehensive analysis enriches our understanding of the molecular mechanisms underlying polyp formation and CRC development, providing potential targets for further investigation and therapeutic intervention. Our findings contribute substantively to crafting personalized strategies for refining the diagnosis and treatment of polyps and CRC.

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“…It is also involved in the regulation of malignancy in various tumors. YKL-40 interacts with a variety of extracellular matrix components and with invasive and metastatic processes of tumor cells in lung cancer, cholangiocarcinoma, endometrial cancer, and other malignancies [ 56 – 58 ]. YKL-40 is an independent risk factor for the occurrence and development of various tumors [ 59 ] and has been used as a marker of tumor growth and inhibition of tumor-cell apoptosis [ 60 ].…”

Section: Discussionmentioning

confidence: 99%

HOXA-AS2 promotes type I endometrial carcinoma via miRNA-302c-3p-mediated regulation of ZFX

et al. 2020

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Background: HOXA cluster antisense RNA2 (HOXA-AS2), a long-chain non-coding RNA, plays an important role in the behavior of various malignant tumors. The roles of HOXA-AS2 in endometrial cancer remain unclear. Methods: We test expression levels of HOXA-AS2, miRNA-302c-3p, the transcription factor zinc finger X-chromosomal protein (ZFX), and the chitinase-like protein YKL-40 in endometrial carcinoma by qRT-PCR and western blotting. Luciferase reporter and qRT-PCR assays were conducted to identify potential binding sites of HOXA-AS2 to miRNA-302c-3p. Cell cycle, migration and invasion ability of endometrial cancer cells were investigated using flow-cytometric analysis, CCK-8 and transwell assays, respectively. Results: HOXA-AS2 levels were significantly increased in endometrial cancer specimens compared to normal endometrial specimens. Upregulated HOXA-AS2 promoted invasion and proliferation of type I endometrial cancer cells. HOXA-AS2 silenced miRNA-302c-3p by binding to it. MiRNA-302c-3p negatively regulates ZFX and YKL-40. Thus HOXA-AS2 promotes the development of type I endometrial cancer via miRNA-302c-3p-mediated regulation of ZFX. Conclusions: These findings suggest that HOXA-AS2 can act as a new therapeutic target for type I endometrial cancer.

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Effects of a Small Interfering RNA Targeting YKL-40 Gene on the Proliferation and Invasion of Endometrial Cancer HEC-1A Cells

Abstract: YKL-40 targeting siRNA specifically blocks the activity of YKL-40 in human EC HEC-1A cells, resulting in tumor suppression. This indicates that YKL-40 might serve as a potential small molecule target in the treatment of EC.

Cited by 10 publications

References 22 publications

Knockdown of YKL‐40 inhibits angiogenesis through regulation of VEGF/VEGFR2 and ERK1/2 signaling in endometrial cancer

Knockdown of YKL‐40 inhibits angiogenesis through regulation of VEGF/VEGFR2 and ERK1/2 signaling in endometrial cancer

Unraveling molecular similarities between colorectal polyps and colorectal cancer: a systems biology approach

HOXA-AS2 promotes type I endometrial carcinoma via miRNA-302c-3p-mediated regulation of ZFX

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