Chromosomal and Genomic Variations in Esophageal Squamous Cell Carcinoma: A Review of Technologies, Applications, and Prospections

Song, Qibin; Jiang, Dongxian; Wang, Shuangfeng; Huang, Jie; Xu, Chen; Hou, Yingyong

doi:10.7150/jca.19601

Cited by 18 publications

(23 citation statements)

References 61 publications

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“…Studies on the molecular mechanisms involved in metastasis of ESCC gathered knowledge that it is associated with epithelial to mesenchymal transition (EMT) and EMT‐related genes and proteins . Other studies found that TP53 gene deletion, epidermal growth factor receptor (EGFR) overexpression, integrin α7, and various other mutations and proteins are associated with distant metastasis in ESCC . However, it is yet unknown how the level of expression of these genes and proteins differs between the initially metastatic and recurrent/progressed ESCC after curative treatment, and how they function in each disease group.…”

Section: Discussionmentioning

confidence: 99%

“…[25][26][27] Other studies found that TP53 gene deletion, epidermal growth factor receptor (EGFR) overexpression, integrin 7, and various other mutations and proteins are associated with distant metastasis in ESCC. [28][29][30] However, it is yet unknown how the level of expression of these genes and proteins differs between the initially metastatic and recurrent/progressed ESCC after curative treatment, and how they function in each disease group. Thus, further researches will be needed to evaluate the underlying biology between the two groups.…”

Section: Discussionmentioning

confidence: 99%

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Impact of sequential lines of palliative chemotherapy in patients with recurrent/metastatic esophageal squamous cell carcinoma: A retrospective analysis of 107 patients at a single center

Kim

Song

et al. 2019

Asia-Pac J Clncl Oncology

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Aim This study was conducted to evaluate the efficacy of palliative chemotherapy by the lines of chemotherapy in recurrent/metastatic esophageal squamous cell carcinoma (ESCC) and to compare the efficacy between the patients with initially metastatic ESCC and those with recurrent/progressed ESCC after curative treatment. Materials and Methods All 107 patients who began palliative chemotherapy for recurrent/metastatic ESCC from March 2015 to October 2017 were included, and grouped according to previous treatment: Groups A (previous chemoradiation alone, n = 30), B (previous surgery alone, n = 11), C (previous chemoradiation and surgery, n = 30), and D (initially metastatic or de novo stage IV, n = 36). Groups A, B, and C (pretreated group) and Group D (treatment‐naïve group) were reorganized according to treatment history. Overall response rate (ORR) and survival data were retrospectively evaluated for each group, lines of chemotherapy, and chemotherapeutic regimen. Results ORR was 25.2%, 7.3%, and 3.4% in first‐, second‐, and third‐line chemotherapy, respectively. The median progression‐free survival (PFS) was 4.7, 2.0, and 2.2 months in first‐, second‐, third‐line chemotherapy, respectively. The median overall survival (OS) after first‐line palliative chemotherapy was 10.1 months, and it was not significantly different between pretreated and treatment‐naive groups. Previous surgery, good performance, ≥3 lines of chemotherapy, and low C‐reactive protein level were linked to a significantly longer OS in multivariate analysis. Conclusion Because PFS rapidly declines with advancement of line of chemotherapy, incorporation of effective treatment modalities in early line treatments is crucial in the management of recurrent/metastatic ESCC. If tolerable, continuing advanced lines of chemotherapy may prolong survival.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Impact of sequential lines of palliative chemotherapy in patients with recurrent/metastatic esophageal squamous cell carcinoma: A retrospective analysis of 107 patients at a single center

Kim

Song

et al. 2019

Asia-Pac J Clncl Oncology

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“…7,22 There are many serological tumor markers in diagnosing and monitoring the malignant tumors. 7,22 There are many serological tumor markers in diagnosing and monitoring the malignant tumors.…”

Section: Discussionmentioning

confidence: 99%

“…5 Furthermore, there are many potential risk factors related to ESCC such as alcohol consumption and smoking, high diets in N-nitroso compounds, low in selenium, fungal toxins, highly salted vitamins A and C, and meats zinc. 7 As a result of, the prognosis and hospital medical effect of the patients is not satisfactory. 7 As a result of, the prognosis and hospital medical effect of the patients is not satisfactory.…”

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confidence: 99%

miR‐32 promotes esophageal squamous cell carcinoma metastasis by targeting CXXC5

Liu

Jiang

et al. 2018

J of Cellular Biochemistry

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MicroRNA‐32 (miR‐32) functioned as a tumor oncogene in some cancer, which control genes involved in important biological and pathological functions and facilitate the tumor growth and metastasis. However, the role of miR‐32 modulates esophageal squamous cell carcinoma (ESCC) malignant transformation has not been clarified. Here, we focused on the function and the underlying molecular mechanism of miR‐32 in ESCC. Results discovered a significant increased expression of miR‐32 in ESCC tissues and cells. Downregulation of miR‐32 inhibited the migration, invasion, adhesion of ESCC cell lines (EC9706 and KYSE450), and the levels of EMT protein in vitro. In vivo, miR‐32 inhibitors decrease tumor size, tumor weight, and the number of metastatic nodules. Hematoxylin and eosin (H&E) results revealed that inhibition of miR‐32 attenuate lung metastasis. Immunohistochemistry and immunofluorescence assay showed increased level of E‐cadherin and decreased level of N‐cadherin and Vimentin with treatment of miR‐32 inhibitors. Furthermore, miR‐32 targeted the 3′‐untranslated region (3′‐UTR) of CXXC5, and inhibited the level of mRNA and protein of CXXC5. There is a negative correlation between the expressions of CXXC5 and miR‐32. Then, after EC9706 and KYSE450 cells cotransfected with si‐CXXC5 and miR‐32 inhibitors, the ability of cell migration, invasion, and adhesion was significantly reduced. In addition, the protein expression of EMT and TGF‐β signaling was also depressed. Collectively, these data supply an insight into the positive role of miR‐32 in ESCC progression and metastasis, and its biological effects may attribute the inhibition of TGF‐β signaling mediated by CXXC5.

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“…ESCC remains one of the most lethal cancers among all malignancies, with a 5-year survival rate of < 20% once diagnosed [6]. Reasons may be the lack of a sensitive method for early detection; thus, detectable regional and distant metastasis have occurred in most ESCC patients at the time of diagnosis [7,8], and the limited clinical staging criteria lacks signi cant molecular biomarkers to effectively stratify patients for treatment options [9].…”

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confidence: 99%

Thermal stress involved in TRPV2 promotes tumorigenesis through the pathway of PI3K/Akt/mTOR in esophageal squamous cell carcinoma

Huang¹,

Li²,

Tian³

et al. 2020

Preprint

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BackgroundEsophageal squamous cell carcinoma (ESCC) is a leading cause of cancer death worldwide. Although the exposure of esophageal mucosa to heat stimuli has long been recognized as an important risk for the initiation and development of ESCC, its underlying mechanisms remain uncharacterized. MethodsWestern blotting and immunofluorescence were used to detect the expression and localization of transient receptor potential vanilloid receptor 2 (TRPV2) in the ESCC cells. The cancerous behaviors of the ESCC cells were evaluated by a single-cell culturing assay, a wound healing assay, a 3D culturing assay and a tube formation assay respectively. In vivo tumorigenicity and metastasis of the ESCC cells were examined via xenograft nude mouse models. Western blotting and IHC were performed to determine the expression profiles of TRPV2 in the ESCC patient tissues. TRPV2 knocked-out ESCC cell line was established using CRISPR-Cas9 gene editing technique.ResultsHere, we found that the expression of TRPV2, one of the thermally sensitive TRP family members, was upregulated in both ESCC cells and clinical samples. We further showed that activation of TRPV2 by recurrent acute thermal stress (54°C, a temperature unexpectedly much lower than those in many dietary modalities) or O1821 (20 μM), a TRPV2 agonist, promoted cancerous behaviors in ESCC cells. The proangiogenic capacity of the heat-challenged ESCC cells was also found to be enhanced profoundly in the tube formation assay; both tumor formation and metastasis that originated from the cells were substantially promoted in nude mouse models upon the activation of TRPV2. These effects were inhibited significantly by tranilast (120 μM), a TRPV2 inhibitor, and abolished by TRPV2 knock-out using CRISPR-Cas9 gene editing. Conversely, overexpression of TRPV2 by transfection of TRPV2 DNA into NE2 cells, could switch the cells to tumorigenesis upon activation of TRPV2. Mechanistically, the driving role of TRPV2 in the progression of ESCC is mainly regulated by the PI3K/Akt/mTOR signaling pathway. Application of a pan-PI3K/mTOR inhibitor and/or a PTEN activator resulted in markedly reduced ESCC cell proliferation. ConclusionsOur study first proved that TRPV2 plays an important role in the tumorigenesis of ESCC upon thermal stress. We revealed that TRPV2-PI3K/Akt/mTOR is a novel and promising target for the prevention and treatment of ESCC.

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Chromosomal and Genomic Variations in Esophageal Squamous Cell Carcinoma: A Review of Technologies, Applications, and Prospections

Cited by 18 publications

References 61 publications

Impact of sequential lines of palliative chemotherapy in patients with recurrent/metastatic esophageal squamous cell carcinoma: A retrospective analysis of 107 patients at a single center

Impact of sequential lines of palliative chemotherapy in patients with recurrent/metastatic esophageal squamous cell carcinoma: A retrospective analysis of 107 patients at a single center

miR‐32 promotes esophageal squamous cell carcinoma metastasis by targeting CXXC5

Thermal stress involved in TRPV2 promotes tumorigenesis through the pathway of PI3K/Akt/mTOR in esophageal squamous cell carcinoma

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