scholarly journals IL-32 Promotes the Radiosensitivity of Esophageal Squamous Cell Carcinoma Cell through STAT3 Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Zhiyu Ma ◽  
Zhen Dong ◽  
Dingyue Yu ◽  
Mingchen Mu ◽  
Wanwen Feng ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Western Blot ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Colony Formation ◽  
Colony Formation Assay ◽  
Stat3 Pathway ◽  
Apoptotic Protein

Objective. This study is set out to determine the relationship between IL-32 and radiosensitivity of esophageal squamous cell carcinoma (ESCC). Methods. Western blot was adopted for measuring IL-32 expression in Eca-109 and TE-10 cells. Eca-109 and TE-10 cells with interference or overexpression of IL-32 were treated with the presence or absence of X-ray irradiation. Then, the use of CCK8 assay was to detect proliferation ability, and effects of IL-32 expression on radiosensitivity of ESCC were tested by colony formation assay. The cell apoptosis was detected using flow cytometry. STAT3 and p-STAT expression, and apoptotic protein Bax were detected by western blot. Results. Colony formation assay and CCK8 assay showed that compared with the NC group without treatment, the growth of the ESCC cells, that is Eca-109 and TE-10, was significantly inhibited in the OE+IR group with highly expressed IL-32 and irradiation. In flow cytometry analysis, in Eca-109 and TE-10 cells, highly expressed IL-32 combined with irradiation significantly increased apoptosis compared with the control group. Highly expressed IL-32 has a synergistic effect with irradiation, inhibiting STAT3 and p-STAT3 expression and increasing apoptotic protein Bax expression. Conclusion. IL-32 can improve the radiosensitivity of ESCC cells by inhibiting the STAT3 pathway. Therefore, IL-32 can be used as a new therapeutic target to provide a new attempt for radiotherapy of ESCC.

Circular RNA hsa_circ_0000654 promotes esophageal squamous cell carcinoma progression by regulating the miR‐149‐5p/IL‐6/STAT3 pathway

IUBMB Life ◽  
2019 ◽  
Vol 72 (3) ◽  
pp. 426-439 ◽  
Author(s):  
Zhiqiao Xu ◽  
Xiaojing Tie ◽  
Ning Li ◽  
Zhenying Yi ◽  
Fengqian Shen ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Circular Rna ◽  
Stat3 Pathway

scholarly journals Downregulation of AAA-domain-containing protein 2 restrains cancer stem cell properties in esophageal squamous cell carcinoma via blockade of the Hedgehog signaling pathway

2020 ◽  
Vol 319 (1) ◽  
pp. C93-C104
Author(s):  
Nuo Li ◽  
Yang Yu ◽  
Baoming Wang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Stem Cell ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cancer Stem Cell ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Squamous Cell ◽  
Colony Formation ◽  
Hedgehog Signaling ◽  
Hedgehog Signaling Pathway

Esophageal squamous cell carcinoma (ESCC) ranks among the five most common cancers in China and has a five-year survival rate of less than 15%. The transcription factor ATPase-family AAA-domain-containing protein 2 (ATAD2) has potential as a therapeutic target in various tumors, and microarray-based gene expression profiling reveals dysregulation of ATAD2 specifically in ESCC. Here we investigated whether ATAD2 could mediate a regulation of cancer stem cell (CSC) biological functions in ESCC. Immunohistochemical staining, reverse transcription quantitative polymerase chain reaction, and Western blot assays all revealed upregulation of ATAD2 in ESCC tissues and cell lines, which furthermore correlated with progression of ESCC. In loss-of-function experiments, silencing of ATAD2 inhibited activation of the Hedgehog signaling pathway, as indicated by reduced expression of glioma-associated oncogene family zinc finger 1 (Gli1), smoothened frizzled class receptor (SMO), and patched 1 (PTCH1). Investigations with 5-ethynyl-2′-deoxyuridine (EdU), Transwell assay, scratch test, flow cytometry, and colony formation assay showed that silencing of ATAD2 or inhibiting the Hedgehog signaling decreased the proliferation, invasion, and migration abilities along with colony formation, but elevated the apoptosis rate of CSCs. Furthermore, in vivo experiments validated the suppressive effect of siRNA-mediated ATAD2 silencing on tumor growth in nude mice. Thus, downregulation of ATAD2 can seemingly restrain the malignant phenotypes of ESCC cells through inhibition of the Hedgehog signaling pathway.

scholarly journals EIF3H promotes aggressiveness of esophageal squamous cell carcinoma by modulating Snail stability

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Xiaobin Guo ◽  
Rui Zhu ◽  
Aiping Luo ◽  
Honghong Zhou ◽  
Fang Ding ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Colony Formation ◽  
Tumor Growth And Metastasis

Abstract Background Overexpression of eukaryotic translation initiation factor 3H (EIF3H) predicts cancer progression and poor prognosis, but the mechanism underlying EIF3H as an oncogene remains unclear in esophageal squamous cell carcinoma (ESCC). Methods TCGA database and the immunohistochemistry (IHC) staining of ESCC samples were used and determined the upregulation of EIF3H in ESCC. CCK8 assay, colony formation assay and transwell assay were performed to examine the ability of cell proliferation and mobility in KYSE150 and KYSE510 cell lines with EIF3H overexpression or knockdown. Xenograft and tail-vein lung metastatic mouse models of KYSE150 cells with or without EIF3H knockdown were also used to confirm the function of EIF3H on tumor growth and metastasis in vivo. A potential substrate of EIF3H was screened by co-immunoprecipitation assay (co-IP) combined with mass spectrometry in HEK293T cells. Their interaction and co-localization were confirmed using reciprocal co-IP and immunofluorescence staining assay. The function of EIF3H on Snail ubiquitination and stability was demonstrated by the cycloheximide (CHX) pulse-chase assay and ubiquitination assay. The correlation of EIF3H and Snail in clinical ESCC samples was verified by IHC. Results We found that EIF3H is significantly upregulated in esophageal cancer and ectopic expression of EIF3H in ESCC cell lines promotes cell proliferation, colony formation, migration and invasion. Conversely, genetic inhibition of EIF3H represses ESCC tumor growth and metastasis in vitro and in vivo. Moreover, we identified EIF3H as a novel deubiquitinating enzyme of Snail. We demonstrated that EIF3H interacts with and stabilizes Snail through deubiquitination. Therefore, EIF3H could promote Snail-mediated EMT process in ESCC. In clinical ESCC samples, there is also a positive correlation between EIF3H and Snail expression. Conclusions Our study reveals a critical EIF3H-Snail signaling axis in tumor aggressiveness in ESCC and provides EIF3H as a promising biomarker for ESCC treatment.

Irradiated esophageal squamous cell carcinoma cells induced the increase of Treg by TGF-beta.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e16092-e16092
Author(s):  
Yuan Wang ◽  
Tao Li ◽  
Jiahua Lv ◽  
Ling Xiao
Keyword(s):  
Flow Cytometry ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Treg Cells ◽  
Carcinoma Cells ◽  
Irradiation Group ◽  
The Difference ◽  
Tgf Β1

e16092 Background: The infiltration of CD4+CD25+Foxp3+ regulatory T cells (Treg) in the tumor microenvironment is one of the main reasons for radiation resistance and tumor recurrence after radiotherapy. It has been established that Treg is more resistant to radiation than other T cells, but the proliferation of immune cells after radiotherapy is affected by other factors, including tumor cells. Treg frequency in the tumor microenvironment after radiotherapy has not been defined. We studied the effect and mechanism of esophageal squamous cell carcinoma on Treg cells after radiation. Methods: After 2Gy irradiation, TE-1 cells were co-cultured with normal peripheral blood lymphocytes for 48 hours. Flow cytometry was used to detect Treg/CD4+T cell frequency. The mRNA expression of TGF-β1/2 in TE-1 was detected by qPCR, and the protein content of TGF-β1/2 in the medium was detected by ELISA. Results: Compared with non-irradiation group, the expression of TGF-β1 and TGF-β2 in TE-1 cells of irradiation group increased, and the protein content of TGF-β1 and TGF-β2 in culture medium increased, the difference was statistically significant(P < 0.001). Flow cytometry showed that CD4+CD25+/CD4+Tcell and CD4+CD25+Foxp3+/CD4+Tcell were increased in the radiotherapy group after co-culture, and the difference was statistically significant(P < 0.001). Conclusions: The expression of TGF-β1 and TGF-β1 in esophageal squamous cell carcinoma cells increased after irradiation, and the frequency of Treg induced by co-culture increased, suggesting that esophageal squamous cell carcinoma cells after radiotherapy can induce the increase of Treg cells, which may be achieved mainly through the mechanism of increasing the secretion of TGF-β1/2.

scholarly journals LncRNA GACAT3 promotes esophageal squamous cell carcinoma progression through regulation of miR-149/FOXM1

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Min Su ◽  
Jinming Tang ◽  
Baihua Zhang ◽  
Desong Yang ◽  
Zhining Wu ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Colony Formation ◽  
Noncoding Rna ◽  
Xenograft Model ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Foxm1 Expression

Abstract Background The long noncoding RNA gastric cancer associated transcript 3 (GACAT3) has been demonstrated to be implicated in the carcinogenesis and progression of many malignancies. However, GACAT3’s levels and role in esophageal squamous cell carcinoma (ESCC) has not been elucidated. Methods GACAT3 amounts were investigated in ESCC tissues and cell lines by qPCR. Its biological functions were examined by CCK-8 assay, colony formation assay, flow cytometry, wound healing assay, transwell assay, and xenograft model establishment. The relationship between GACAT3 and miR-149 was assessed by dual-luciferase reporter assay. Results GACAT3 amounts were elevated in ESCC tissue and cell specimens. Functional studies showed that GACAT3 silencing reduced the proliferation, migration and invasion of cultured ESCC cells, and decreased tumor growth in mice. Furthermore, GACAT could directly interact with miR-149. In addition, colony formation and invasion assays verified that GACAT3 promotes ESCC tumor progression through miR-149. Moreover, GACAT3 acted as a competing endogenous RNA (ceRNA) to modulate FOXM1 expression. Conclusions These findings indicate that GACAT3 functions as an oncogene by acting as a ceRNA for miR-149 to modulate FOXM1 expression in ESCC, suggesting that GACAT3 might constitute a therapeutic target in ESCC.

scholarly journals FLVCR1 Predicts Poor Prognosis and Promotes Malignant Phenotype in Esophageal Squamous Cell Carcinoma via Upregulating CSE1L

2021 ◽  
Vol 11 ◽  
Author(s):  
Suna Zhou ◽  
Mingxin Zhang ◽  
Chao Zhou ◽  
Yinnan Meng ◽  
Haihua Yang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Colony Formation ◽  
Xenograft Model ◽  
Migration And Invasion ◽  
Node Metastasis ◽  
And Migration

ObjectiveDysregulation of feline leukemia virus subgroup C receptor 1(FLVCR1) expression has been investigated in several tumors. However, the expression and role of FLVCR1 in esophageal squamous cell carcinoma (ESCC) remain largely unknown.MethodsFLVCR1 expression in tissues was measured by immunohistochemical staining (IHC). Celigo assay, MTT assay, colony formation, caspase 3/7 activity analysis, wound healing assay, Transwell migration, and invasion assay were applied to assess the effects of FLVCR1 on ESCC tumorigenesis. Coimmunoprecipitation (Co-IP) and liquid chromatography-mass spectrometry (LC-MS) were used to identify protein interactions with FLVCR1. An in vivo imaging system (IVIS) was used to investigate the functions of FLVCR1 on the growth and metastatic capability of ESCC cells in a xenograft model and a tail vein metastasis model.ResultsElevated expression of FLVCR1 was detected in ESCC tissues and predicted poor survival. Upregulated FLVCR1 was positively correlated with lymph node metastasis (N stage) and late tumor-node-metastasis (TNM) stage. FLVCR1 knockdown inhibited cell proliferation and colony formation ability, induced cell apoptosis, and repressed cell migration and invasion of ESCC in vitro. Inhibition of FLVCR1 markedly repressed tumorigenicity and metastasis of ESCC cells in vivo. Mechanistically, chromosome segregation 1–like (CSE1L) was identified to interact with FLVCR1 using a Co-IP assay. Moreover, the inhibitory effect of FLVCR1 knockdown on proliferation and migration was counteracted by the exogenous expression of CSE1L.ConclusionFLVCR1 plays a pivotal role in ESCC cell survival, growth, and migration. These functions may be partially dependent upon the protein interaction between FLVCR1 and CSE1L. In addition, FLVCR1 can be applied as a clinical prognostic marker for patients with ESCC.

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