Up-regulation of SOCS4 promotes cell proliferation and migration in esophageal squamous cell carcinoma

Ying, Jie; Huang, Huan-Huan; Zhang, Miaomiao; Chen, Jinfei

doi:10.21037/tcr-21-700

Cited by 6 publications

(3 citation statements)

References 40 publications

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“…It has been shown that the SOCS family plays an important role in the regulation of cellular responses to cytokines and growth factors, and that the SOCS family is a major negative regulator of a number of signaling pathways, including JAK/STAT pathway [3,20,21] . More and more studies suggested that the SOCS family genes were the key factors in the occurrence, development, invasion and angiogenesis of malignant tumors [2,22] . However, only a limited number of studies have shown that SOCS family member are associated with HCC [23] , and the exact biological function of the SOCS family in HCC remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Expression characteristics, immune signature, and prognostic value of the SOCS family identified by multiomics integrative analysis in liver cancer

Dong

Dai

Fang

et al. 2023

Preprint

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Objective Hepatocellular carcinoma is one of the most common malignancies in the world, and the death rate is very high. The members of the SOCS family are the key factors in the regulation of various cytokines and growth factors. It is not clear, however, whether the level of the SOCS family will affect the prognosis in patients with HCC. Methods Firstly, we studied the expression levels of the SOCS family genes in the HCC and the relationship between the expression level of the SOCS family and different clinicopathological characteristics. Then the public database was used to analyze the changes of expression, potential function, transcription factors and immune invasion of SOCS family members. Finally, we analyzed the prognostic value of the patients with SOC family with HCC and the correlation with SOC family and ferroptosis-related genes. Results The expression of SOCS2-7 and CISH was downregulated in HCC. The SOCS4, SOCS5 and SOCS7 genes were all related to the clinicopathological features of HCC patients. SOCS family genes are mainly related to PIK3R3, GHR, TNS4, TNS4 pathway. We found that STAT3, PPAR-gamma 2 and IRF-2 are important transcription factors in regulating SOCS family members. We also confirmed that the expression level of SOCS family members are closely related to the immune infiltration of liver cancer. Then, we clarified that SOCS2 and SOCS4 are risk-related gene in predicting the prognosis of patients with liver cancer. Finally, we found that SOCS2 gene may be involved in the development and progression of hepatocellular carcinoma, but the mechanism needs further experimental verification. Conclusion Our study may expand upon the understanding of SOCS gene function in liver cancer and help clinicians select appropriate drugs and predict the prognosis of patients with liver cancer.

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Section: Discussionmentioning

confidence: 99%

Expression characteristics, immune signature, and prognostic value of the SOCS family identified by multiomics integrative analysis in liver cancer

Dong

Dai

Fang

et al. 2023

Preprint

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“…Despite the progress achieved in the diagnosis and therapeutic regimens, the 5-year survival rate remains poor in patients with ESCA ( 2 - 4 ). Recurrence and metastasis are the major obstacles that affect the therapeutic efficacy and clinical outcomes for patients with ESCA ( 5 ). Hence, there is an urgent need to unveil the molecular mechanisms involved in the recurrence and metastasis of ESCA, which will help to screen and identify the potential therapeutic targets and pave new ways to enhance the clinical therapeutic efficacy of ESCA treatment.…”

Section: Introductionmentioning

confidence: 99%

SPP1 promotes tumor progression in esophageal carcinoma by activating focal adhesion pathway

Sun,

Tang,

Cai

2024

J Gastrointest Oncol

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Background Recurrence and metastasis are the major obstacles affecting the therapeutic efficacy and clinical outcomes for patients with esophageal carcinoma (ESCA). Secreted phosphoprotein 1 (SPP1) is considered as a hub gene in ESCA and is negatively associated with disease-free survival (DFS) in ESCA. However, the exact roles and underlying mechanisms remain elusive. This study aims to examine the roles of SPP1 on ESCA, and elucidate the potential mechanisms. Methods Bioinformatics were used to analyze the expression of SPP1 in ESCA tissues, and its relations with clinicopathological characteristics and clinical prognosis in patients with ESCA based on The Cancer Genome Atlas (TCGA) dataset. Loss-of-function was conducted to examine the roles of SPP1 on malignant behaviors of ESCA cells by cell counting kit-8 (CCK8), plate clone, wound healing, and transwell assays. Gene set enrichment analysis (GSEA) was conducted to screen the pathways associated with SPP1 in ESCA. Then, the enriched pathway and the underlying mechanism were elucidated by western blotting, cell adhesion, and cell spreading assays. Lastly, Y15 [a specific inhibitor of focal adhesion kinase (FAK)] was used to examine its potential to inhibit tumor growth in ESCA cells. Results SPP1 was upregulated in ESCA tissues compared to the adjacent nontumorous tissues, which was closely associated with clinical stage, lymph node metastasis, histological subtype, and p53 mutation. A high expression of SPP1 indicated a poor clinical prognosis in patients with ESCA. The knockdown of SPP1 inhibited cell proliferative, migratory, and invasive capacities in ESCA cells. GSEA indicated that the focal adhesion pathway was closely related with SPP1 in ESCA. Further studies confirmed that the knockdown of SPP1 suppressed cell adhesion ability and reduced the expression of p-FAK and p-Erk in ESCA cells. In addition, Y15 inhibited FAK autophosphorylation and dramatically inhibited cell proliferation, migration, and invasion in ESCA cells. Conclusions SPP1 promotes tumor progression in ESCA by activating FAK/Erk pathway, and FAK is a potential therapeutic target to overcome tumor recurrence and metastasis of ESCA.

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“…Esophageal cancer (EC) is one of the most common malignant tumors of the upper digestive tract in the world ( 1 ). Recently, the International Agency for Research on Cancer of the World Health Organization reported that in 2020, there were 600,000 new cases of EC and 540,000 EC-related deaths worldwide, making it the 8th most common cancer, and the 6th leading cause of cancer-related deaths ( 2 , 3 ). EC is also one of the top 10 malignant tumors in China, and with 320,000 new cases and 300,000 deaths, it was the 6th most common cancer and the 4th leading cause of cancer-related deaths in 2020 in China ( 4 ).…”

Section: Introductionmentioning

confidence: 99%

Bufalin suppresses esophageal squamous cell carcinoma progression by activating the PIAS3/STAT3 signaling pathway

Ju¹,

Shi²,

Liu³

et al. 2023

J Thorac Dis

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Background: Esophageal cancer, especially esophageal squamous cell carcinoma (ESCC), is a common malignant tumor of the digestive tract. Bufalin is an effective anti-tumor compound. However, little is known about the regulatory mechanisms of Bufalin in ESCC. To investigate the effect and molecular mechanism of Bufalin on the proliferation, migration and invasion of ESCC cells will provide a more reliable basis for the application of Bufalin in clinical tumor therapy.Methods: First, the half-inhibitory concentration (IC50) of Bufalin was evaluated by Cell Counting Kit-8 (CCK-8) assays. In vitro, the effects of Bufalin on the proliferation of the ECA109 cells was measured using CCK-8 and 5-ethynyl-2'-deoxyuridine assays. Wound-healing and transwell assays were used to evaluate the effects of Bufalin on the migration and invasion of the ECA109 cells. Further, to determine the mechanisms underlying the Bufalin-mediated suppression of cell progression in ESCC, total RNA was extracted from negative control (NC) and Bufalin treated cells to perform RNA-sequencing (RNA-seq) to screen for abnormally expressed genes. In vivo, the ECA 109 cells were subcutaneously injected into BALB/c nude mice to determine the effects of Bufalin on tumor cell proliferation. The protein inhibitor of activated signal transducer and activator of transcription 3 (PIAS3), signal transducer and activator of transcription 3 (STAT3), and phosphorylated STAT3 (p-STAT3) protein expression levels in the ECA109 cells were detected by Western blot. Results:The CCK-8 assays showed that the IC50 of Bufalin was 200 nM. The proliferation, migration, and invasion ability of the ECA109 cells was significantly inhibited in the Bufalin group in a concentrationdependent manner. In vivo, the Xenograft tumor model showed that Bufalin decreased the tumor volume and weight of the subcutaneous tumors. The RNA-seq results showed that the expression of PIAS3 was upregulated in the Bufalin group. Additionally, down-regulation of PIAS3 decreased the inhibition of STAT3, thereby increasing p-STAT3 expression. Finally, PIAS3 knockdown reversed the inhibitory effects of Bufalin on the proliferation, migration, and invasion of the ECA109 cells.Conclusions: Bufalin may inhibit the proliferation, migration, and invasion of the ECA109 cells through the PIAS3/STAT3 signaling pathway.

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Up-regulation of SOCS4 promotes cell proliferation and migration in esophageal squamous cell carcinoma

Cited by 6 publications

References 40 publications

Expression characteristics, immune signature, and prognostic value of the SOCS family identified by multiomics integrative analysis in liver cancer

Expression characteristics, immune signature, and prognostic value of the SOCS family identified by multiomics integrative analysis in liver cancer

SPP1 promotes tumor progression in esophageal carcinoma by activating focal adhesion pathway

Bufalin suppresses esophageal squamous cell carcinoma progression by activating the PIAS3/STAT3 signaling pathway

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