Endothelial cell-specific molecule 1 drives cervical cancer progression

Lü, Jingjing; Liu, Qin; Zhu, Lixia; Liu, Yuanyuan; Zhu, Xiao-Ren; Peng, Shi-Qing; Chen, Min-Bin; Li, Ping

doi:10.1038/s41419-022-05501-5

Cited by 15 publications

(11 citation statements)

References 59 publications

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“…The study notably signifies the first in-depth exploration of ESM1’s role in PTC, emphasizing its overexpression and critical involvement in cell proliferation and migration. Following ESM1 inhibition via shRNA, we observed decreased cellular growth and increased apoptosis rates, supporting ESM1’s value as a therapeutic target [ 21 – 24 ]. The profound impact of ESM1 knockdown on cellular mechanisms not only bolsters its position as a viable prognostic biomarker but also as a potential therapeutic agent in thyroid cancer.…”

Section: Discussionmentioning

confidence: 67%

Functional analysis of ESM1 by shRNA-mediated knockdown of its expression in papillary thyroid cancer cells

Xie,

He,

Zhang

et al. 2024

PLoS ONE

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Objective Endothelial specific molecule-1 (ESM1) is implicated as an oncogene in multiple human cancers. However, the function of ESM1 in papillary thyroid cancer (PTC) is not well understood. The current study aimed to investigate the effect of ESM1 on the growth, migration, and invasion of PTC to provide a novel perspective for PTC treatment. Methods The expression levels of ESM1 in PTC tissues form 53 tumor tissue samples and 59 matching adjacent normal tissue samples were detected by immunohistochemical analysis. Knockdown of ESM1 expression in TPC-1 and SW579 cell lines was established to investigate its role in PTC. Moreover, cell proliferation, apoptosis, wound healing, and transwell assays were conducted in vitro to assess cell proliferation, migration and invasion. Results The findings revealed that ESM1 expression was significantly higher in PTC tissues than that found in paraneoplastic tissues (P<0.0001). Knockdown of ESM1 expression inhibited the proliferation, migration, and invasion of TPC-1 and SW579 cells in vitro. Compared with the control group, the mRNA and protein levels of ESM1 in PTC cells were significantly reduced following knockdown of its expression (P<0.01). In addition, ESM1-knockdown cells indicated decreased proliferation and decreased migratory and invasive activities (P<0.01, P<0.01, P<0.001, respectively). Conclusions ESM1 was identified as a major gene in the occurrence and progression of PTC, which could increase the proliferation, migration, and invasion of PTC cells. It may be a promising diagnostic and therapeutic target gene.

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Section: Discussionmentioning

confidence: 67%

Functional analysis of ESM1 by shRNA-mediated knockdown of its expression in papillary thyroid cancer cells

Xie,

He,

Zhang

et al. 2024

PLoS ONE

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show abstract

“…Recent studies have revealed that ESM1 is highly expressed in a variety of malignancies, including lung, kidney, liver, breast, and brain glioblastoma and that it is associated with tumor angiogenesis, metastasis, and poor prognosis (22)(23). However, to the best of our knowledge, its role on the proliferation and migration of thyroid cancer cells has not been previously explored.…”

Section: Discussionmentioning

confidence: 99%

Functional analysis of ESM1 by shRNA-mediated knockdown of its expression in papillary thyroid cancer cells

Xie

Wang

et al. 2023

Preprint

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Endothelial specific molecule-1 (ESM1) is implicated as an oncogene in multiple human cancers. However, the function of ESM1 in papillary thyroid cancer (PTC) is not well understood. The current study aimed to investigate the effect of ESM1 on the growth, migration, and invasion of PTC to provide a novel perspective for PTC treatment. The expression levels of ESM1 in PTC tissues were detected by immunohistochemical analysis. Knockdown of ESM1 expression in TPC-1 and SW579 cell lines was established to investigate its role in PTC. Moreover, cell proliferation, apoptosis, wound healing, and transwell assays were conducted in vitro to assess cell proliferation, migration and invasion. The findings revealed that ESM1 expression was significantly higher in PTC tissues than that found in paraneoplastic tissues. Knockdown of ESM1 expression inhibited the proliferation, migration, and invasion of TPC-1 and SW579 cells in vitro. Compared with the control group, the mRNA and protein levels of ESM1 in PTC cells were significantly reduced following knockdown of its expression. In addition, ESM1-knockdown cells indicated decreased proliferation and decreased migratory and invasive activities. Overall, ESM1 was identified as a major gene in the occurrence and progression of PTC, which could increase the proliferation, migration, and invasion of PTC cells. It may be a promising diagnostic and therapeutic target gene.

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“…For instance, Li YK et al showed that ESM1 overexpression facilitated cell proliferation, migration, and angiogenesis in ovarian cancer cells via the Akt pathway 38 . Furthermore, Lu JJ et al revealed that ESM1 augmented the PI3K signaling pathway and accelerated EMT in cervical cancer 39 . Compared to these results, our research harbored the following differences: Firstly, we studied the clinical correlation between ESM1 and CSCC patients based on clinical sample studies and bioinformatics analysis of the TCGA database; The conclusions are consistent with previous studies; Then, through in vitro experiments, a preliminary study was conducted on the expression of ESM1 through VEGFα/VEGFR2/ERK and hypoxia-related signaling pathways regulate tumor microvascular formation; The different molecular mechanism compared to previous studies suggested that ESM1 might participate in the occurrence and development of CSCC through multiple avenues.…”

Section: Discussionmentioning

confidence: 99%

Targeting ESM1/ VEGFα signaling axis: a promising therapeutic avenue for angiogenesis in cervical squamous cell carcinoma

Li¹,

Su²,

Xue³

et al. 2023

J. Cancer

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Background: Endothelial-specific molecule 1 (ESM1) dysregulation is widespread in various malignancies. However, the exact significance of ESM1 in cervical squamous cell carcinoma (CSCC) is not yet well understood. Methods: The expression of ESM1 in CSCC was probed by immunohistochemistry (IHC) assay using human specimens and validated and explored ESM1 in CSCC based on TNMplot and TCGA (The Cancer Genome Atlas Program) data repository. Further, the GSEA analysis and in vitro experiments of human CSCC cell lines, including SiHa and ME-180, were performed to investigate the masked molecular mechanisms of ESM1 in CSCC. Results: ESM1 was overexpressed in clinical CSCC tissues compared with paracancer controls, was an independent prognostic factor and was associated with poor prognosis in CSCC patients. These findings were further confirmed in the TNMplot and TCGA datasets. Furthermore, GSEA analysis revealed that the ESM1 high expression group was significantly enriched in carcinoma angiogenesis and the VEGFα signaling pathway. In addition, in vitro assays with human CSCC cell lines, including SiHa and ME-180, demonstrated that knockdown of ESM1 expression inhibited tumor cell proliferation, migration and invasion, resulting in attenuated VEGFα expression and blocked phosphorylation of VEGFR2 and ERK-1/2. Conclusion: In CSCC patients, ESM1 was considerably overexpressed. Upregulation of ESM1 is predictive of poor clinical outcomes in CSCC. Furthermore, ESM1 overexpression promoted carcinoma angiogenesis and CSCC progression through the VEGF/ERK signaling pathway. Hence, ESM1 and associated genes might be useful prognostic biomarkers or therapeutic targets for CSCC individuals.

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Endothelial cell-specific molecule 1 drives cervical cancer progression

Cited by 15 publications

References 59 publications

Functional analysis of ESM1 by shRNA-mediated knockdown of its expression in papillary thyroid cancer cells

Functional analysis of ESM1 by shRNA-mediated knockdown of its expression in papillary thyroid cancer cells

Functional analysis of ESM1 by shRNA-mediated knockdown of its expression in papillary thyroid cancer cells

Targeting ESM1/ VEGFα signaling axis: a promising therapeutic avenue for angiogenesis in cervical squamous cell carcinoma

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