Foxhead box D1 promotes the partial epithelial-to-mesenchymal transition of laryngeal squamous cell carcinoma cells via transcriptionally activating the expression of zinc finger protein 532

Fan, Li; Jin-xiu, Wang; Pingping, Deng; Wang, Yuanyuan; Zhang, Aiping; Yang, Mengsheng; Zeng, Gang

doi:10.1080/21655979.2021.2024978

Cited by 14 publications

(8 citation statements)

References 45 publications

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“…More importantly, the results showed that FHL2 had higher expression in A549 and NCI‐H460 cells, and lower expression in NCI‐H292 and H1299 cells (Figure 2B,C, p <.05 or p <.01). In order to better reflect the effects of FHL2 interference and overexpression, A549 and NCI‐H460 cells were selected to perform FHL2 knockdown, while NCI‐H292 and H1299 cells were used to carry out FHL2 overexpression referring to earlier studies 19,20 . FHL2 knockdown was carried out by transfecting with the sequences of shRNA‐NC, FHL2‐shRNA1, 2, 3 into A549 and NCI‐H460 cells, respectively.…”

Section: Resultsmentioning

confidence: 99%

“…In order to better reflect the effects of FHL2 interference and overexpression, A549 and NCI-H460 cells were selected to perform FHL2 knockdown, while NCI-H292 and H1299 cells were used to carry out FHL2 overexpression referring to earlier studies. 19,20 FHL2 knockdown was carried out by transfecting with the sequences of shRNA-NC, FHL2-shRNA1, 2, 3 into A549 and NCI-H460 cells, respectively. Considering that FHL2-shRNA1 has the best interference effect, it was selected for further follow-up research.…”

Section: Fhl2 Was Markedly Upregulated In Nsclc Tissues and Cellsmentioning

confidence: 99%

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High level of FHL2 exacerbates the outcome of non‐small cell lung cancer (NSCLC) patients and the malignant phenotype in NSCLC cells

Zhang

et al. 2022

Int J Experimental Path

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Non-small cell lung cancer (NSCLC) is a malignant tumour with high mortality.FHL2 has been identified as a biomarker of lung cancer. This research explored the effects of FHL2 expression on NSCLC. NSCLC-associated data sets were collected from the assistant for clinical bioinformatics and TCGA databases respectively. The association between FHL2 and clinical characteristics, the prognostic significance of FHL2 and the influences of various variables on NSCLC were determined by Pearson's chi-squared test, the Kaplan-Meier curve and the Cox regression model respectively. FHL2 level was altered by cell transfection and was measured by qRT-PCR. Tumour xenograft formation was completed by inoculating sh-FHL2/pcDNA-FHL2 transfected cells into BALB/c nude mice. Protein expression was assessed by western blot. Cell apoptosis, proliferation and epithelial -mesenchymal transition (EMT) characteristics were evaluated employing TUNEL, BrdU + and microscopic observation respectively. The expression of Ki67 and N-cadherin was assessed by immunohistochemistry. The results showed that FHL2 was highly expressed in NSCLC tissues. Patients with high FHL2 expression experienced lower overall survival probability. FHL2 knockdown promoted apoptosis, but inhibited EMT of A549 and NCI-H460 cells, which was verified by the increased ratios of cleaved caspase 9/caspase 9 and cleaved caspase 3/caspase 3, as well as augmented E-cadherin and reduced N-cadherin. In an in vivo assay FHL2 knockdown decreased tumour volume and weight, repressed EMT, but enhanced apoptosis. FHL2 upregulation showed the opposite effects of FHL2 knockdown. Furthermore, FHL2 upregulation facilitated cell proliferation both in in vitro and in vivo assays. These outcomes indicated that high level of FHL2 facilitated tumorigenesis, as well as the proliferation and EMT of NSCLC cells.

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Section: Resultsmentioning

confidence: 99%

Section: Fhl2 Was Markedly Upregulated In Nsclc Tissues and Cellsmentioning

confidence: 99%

High level of FHL2 exacerbates the outcome of non‐small cell lung cancer (NSCLC) patients and the malignant phenotype in NSCLC cells

Zhang

et al. 2022

Int J Experimental Path

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“…Moreover, COLEC12 as a cancer stemness-related signature could predict colon adenocarcinoma prognosis [ 28 ]. At an epithelial cellular level, activation of ZNF532 could promote the epithelial-to-mesenchymal transition in laryngeal squamous cell carcinoma cells [ 29 ]. We observed that COLEC12 and ZNF532 were highly expressed in macrophages and endothelial cells, respectively, which was consistent with the findings that COLEC12 expression was correlated with immune-related molecules [ 30 ], and ZNF532 altered the biological activity of endothelial cells [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Cancer-Associated Fibroblast Risk Model for Prediction of Colorectal Carcinoma Prognosis and Therapeutic Responses

Wang

Chen

Zhao

et al. 2023

Mediators of Inflammation

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Colorectal carcinoma (CRC) is a malignant tumor of the digestive system. Cancer-associated fibroblasts (CAFs) are important cellular elements in the tumor microenvironment of CRC, which contribute to CRC progression and immune escape. To predict the survival outcome and therapeutic responses of CRC patients, we identified genes connected with stromal CAF and generated a risk model. In this study, we used multiple algorithms to reveal CAF-related genes in the Gene Expression Omnibus and The Cancer Genome Atlas datasets and construct a risk model composed by prognostic CAF-associated genes. Then, we evaluated whether the risk score could predict CAF infiltrations and immunotherapy in CRC and confirmed the expression of the risk model in CAFs. Our results showed that CRC patients with high CAF infiltrations and stromal score had worse prognosis than those with low-CAF infiltrations and stromal score. We obtained 88 stromal CAF-associated hub-genes and generated a CAF risk model consisting of ZNF532 and COLEC12. Compared with low-risk group, the overall survival in high-risk group was shorter. The relationship between risk score, ZNF532 and COLEC12, and stromal CAF infiltrations and CAF markers was positive. In addition, the effect of immunotherapy in the high-risk group was not as good as that in the low-risk group. Patients with the high-risk group were enriched in chemokine signaling pathway, cytokine-cytokine receptor interaction, and focal adhesion. Finally, we confirmed that the expressions of ZNF532 and COLEC12 in risk model were widely distributed in fibroblasts of CRC, and the expression levels were higher in fibroblasts than CRC cells. In conclusion, the prognostic CAF signature of ZNF532 and COLEC12 can be applied not only to predict the prognosis of CRC patients but also to evaluate the immunotherapy response in CRC patients, and these findings provide the possibility for further development of individualized treatment for CRC.

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“…Notably, only such hybrid cells can express CD44+ surface-glycoproteins that characterize stem cells [ 163 ]. The concept of p-EMT and its potential metastatic benefits has also been described in studies on head and neck carcinomas [ 164 , 165 , 166 , 167 ]. More importantly, p-EMT has been shown to be related to detrimental clinical effects: a higher p-EMT score was found to be related to lymph node metastasis and is associated with advanced lymph node staging in head and neck squamous cell carcinoma (HNSCC) [ 168 ].…”

Section: Epithelial-to-mesenchymal Transition—the Contemporary Approachmentioning

confidence: 99%

Epithelial-to-Mesenchymal Transition in Metastasis: Focus on Laryngeal Carcinoma

Goulioumis

Gyftopoulos²

2022

Biomedicines

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In epithelial neoplasms, such as laryngeal carcinoma, the survival indexes deteriorate abruptly when the tumor becomes metastatic. A molecular phenomenon that normally appears during embryogenesis, epithelial-to-mesenchymal transition (EMT), is reactivated at the initial stage of metastasis when tumor cells invade the adjacent stroma. The hallmarks of this phenomenon are the abolishment of the epithelial and acquisition of mesenchymal traits by tumor cells which enhance their migratory capacity. EMT signaling is mediated by complex molecular pathways that regulate the expression of crucial molecules contributing to the tumor’s metastatic potential. Effectors of EMT include loss of adhesion, cytoskeleton remodeling, evasion of apoptosis and immune surveillance, upregulation of metalloproteinases, neovascularization, acquisition of stem-cell properties, and the activation of tumor stroma. However, the current approach to EMT involves a holistic model that incorporates the acquisition of potentials beyond mesenchymal transition. As EMT is inevitably associated with a reverse mesenchymal-to-epithelial transition (MET), a model of partial EMT is currently accepted, signifying the cell plasticity associated with invasion and metastasis. In this review, we identify the cumulative evidence which suggests that various aspects of EMT theory apply to laryngeal carcinoma, a tumor of significant morbidity and mortality, introducing novel molecular targets with prognostic and therapeutic potential.

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Foxhead box D1 promotes the partial epithelial-to-mesenchymal transition of laryngeal squamous cell carcinoma cells via transcriptionally activating the expression of zinc finger protein 532

Cited by 14 publications

References 45 publications

High level of FHL2 exacerbates the outcome of non‐small cell lung cancer (NSCLC) patients and the malignant phenotype in NSCLC cells

High level of FHL2 exacerbates the outcome of non‐small cell lung cancer (NSCLC) patients and the malignant phenotype in NSCLC cells

Cancer-Associated Fibroblast Risk Model for Prediction of Colorectal Carcinoma Prognosis and Therapeutic Responses

Epithelial-to-Mesenchymal Transition in Metastasis: Focus on Laryngeal Carcinoma

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