scholarly journals Serglycin promotes proliferation, migration, and invasion via the JAK/STAT signaling pathway in osteosarcoma

Aging ◽  
2021 ◽  
Vol 13 (17) ◽  
pp. 21142-21154
Author(s):  
Bin Lv ◽  
Guangyu Gao ◽  
Yuhong Guo ◽  
Zhiping Zhang ◽  
Renfeng Liu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Migration And Invasion ◽  
Stat Signaling

Dexmedetomidine Inhibited Proliferation and Invasion of Cervical Cancer Cells by Inhibiting the Janus Tyrosine Kinase/Signal Transducer and Activator of Transcription Signaling Pathway

2021 ◽  
Vol 11 (7) ◽  
pp. 1293-1304
Author(s):  
FenLan Xu ◽  
Liying Xu ◽  
Xiaoyan Xu ◽  
Zhenhua Huang ◽  
Liang Su
Keyword(s):  
Cervical Cancer ◽  
Cell Migration ◽  
Western Blot ◽  
Cell Viability ◽  
Signaling Pathway ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Stat Signaling ◽  
Related Proteins

The role of anesthetics in the treatment of cancer has been reported, but the role of Dexmedetomidine (Dex) in the treatment of cervical cancer (CC) has not been reported.In this study, cell viability and proliferation were determined by MTT and cloning formation assay. The expression of proliferation-related proteins ki67 and PCNA was detected by western blot. Wound healing and transwell detected cell migration and invasion, and western blot detected the expression of migration and invasion related proteins MMP4 and MMP9, and epithelial-mesenchymal transformation (ETM)-related proteins N-cadherin, Snail, Vimentin and E-cadherin. Western blot also detected the expression of pathway related proteins p-JAK2, p-STAT1, p-STAT3, JAK2, STAT1 and STAT3. It showed that Dex inhibited the cell viability and proliferation of Hela and siHa and the expression of ki67 and PCNA were also inhibited. Dex inhibited the cell migration and invasion, and inhibited the expression of MMP4 and MMP9. In addition, Dex inhibited the expression of N-cadherin, Snail and Vimentin, and promoted the expression of E-cadherin. Dex inhibited the expression of p-JAK2, p-STAT1 and p-STAT3. After the addition of JAK/STAT signaling pathway agonist IL-6, the inhibition of Dex on proliferation, migration and invasion of CC cells was reversed. And the addition of JAK/STAT signaling pathway inhibitor AG490 could counteract the excitatory effect of IL-6 on the pathway, at which time the cell proliferation, invasion and migration were significantly increased. In conclusion, our study demonstrated that Dex inhibited proliferation, migration, and invasion of cells in CC by blocking the JAK/STAT signaling pathway.

scholarly journals Preliminary study on the role and mechanism of KIRREL3 in the development of esophageal squamous cell carcinoma (ESCC)

2022 ◽  
Author(s):  
Bingbing Yang ◽  
Xiane Zhang ◽  
Hao Zhou ◽  
Xiaoyan Zhang ◽  
Wanjing Yang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Squamous Cell ◽  
Tumor Formation ◽  
Migration And Invasion ◽  
Stat Signaling

Abstract Background: Esophageal squamous cell carcinoma (ESCC) is a common malignant tumor of the digestive tract, which is very harmful to human health. The JAK-STAT signaling pathway is a recognized carcinogenic pathway that plays a role in the proliferation, apoptosis, migration, and invasion of a variety of cancer cells. Some studies have shown that the activation status of STAT3 affects the expression of KIRREL3. However, the expression of KIRREL3 in ESCC and its relationship with KIRREL3 or the JAK-STAT signaling pathway is still unclear.Methods: In this study, we used immunohistochemistry and western blotting to analyze the protein expression levels of KIRREL3 in tumor tissues and ESCC cell lines. We applied proliferation assays, plate clone formation assays, Transwell assays, flow cytometry analysis, and CDX animal models to examine the role of KIRREL3 in ESCC.Results: The results indicate that KIRREL3 is highly expressed to varying degrees in ESCC tissues and cell lines. Knocking down KIRREL3 expression in ESCC cells could correspondingly inhibit cell proliferation, colony formation, invasion, and migration, and had some effects on cell cycle progression and apoptosis. In addition, overexpressing KIRREL3 in these cells had opposite effects. Tumor formation in nude mice experiments also confirmed that KIRREL3 is involved in the growth of ESCC cells in vivo.Conclusions: These data suggest that KIRREL3 plays a key role in the development of ESCC, and KIRREL3 is a potential new target for the early diagnosis and clinical treatment of this disease.

PYCR1 knockdown inhibits the proliferation, migration, and invasion by affecting JAK/STAT signaling pathway in lung adenocarcinoma

2020 ◽  
Vol 59 (5) ◽  
pp. 503-511 ◽  
Author(s):  
Yawen Gao ◽  
Lihua Luo ◽  
Yangchun Xie ◽  
Yu Zhao ◽  
Jie Yao ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Migration And Invasion ◽  
Stat Signaling

scholarly journals ST8SIA1 inhibits the proliferation, migration and invasion of bladder cancer cells by blocking the JAK/STAT signaling pathway

2021 ◽  
Vol 22 (4) ◽  
Author(s):  
Shengjin Yu ◽  
Shidan Wang ◽  
Xiaoxin Sun ◽  
Yinshuang Wu ◽  
Jun Zhao ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Migration And Invasion ◽  
Bladder Cancer Cells ◽  
Stat Signaling

scholarly journals Preliminary Study on the Role and Mechanism of KIRREL3 in the Development of Esophageal Squamous Cell Carcinoma (ESCC)

2021 ◽  
Author(s):  
Bingbing Yang ◽  
Xiane Zhang ◽  
Hao Zhou ◽  
Xiaoyan Zhang ◽  
Wanjing Yang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Squamous Cell ◽  
Tumor Formation ◽  
Migration And Invasion ◽  
Stat Signaling

Abstract Background: Esophageal squamous cell carcinoma (ESCC) is a common malignant tumor of the digestive tract, which is very harmful to human health. The JAK-STAT signaling pathway is a recognized carcinogenic pathway that plays a role in the proliferation, apoptosis, migration, and invasion of a variety of cancer cells. Some studies have shown that the activation status of STAT3 affects the expression of KIRREL3. However, the expression of KIRREL3 in ESCC and its relationship with KIRREL3 or the JAK-STAT signaling pathway is still unclear.Methods: In this study, we used immunohistochemistry and western blotting to analyze the protein expression levels of KIRREL3 in tumor tissues and ESCC cell lines. We applied proliferation assays, plate clone formation assays, Transwell assays, flow cytometry analysis, and CDX animal models to examine the role of KIRREL3 in ESCC.Results: The results indicate that KIRREL3 is highly expressed to varying degrees in ESCC tissues and cell lines. Knocking down KIRREL3 expression in ESCC cells could correspondingly inhibit cell proliferation, colony formation, invasion, and migration, and had some effects on cell cycle progression and apoptosis. In addition, overexpressing KIRREL3 in these cells had opposite effects. Tumor formation in nude mice experiments also confirmed that KIRREL3 is involved in the growth of ESCC cells in vivo. Conclusions: These data suggest that KIRREL3 plays a key role in the development of ESCC, and KIRREL3 is a potential new target for the early diagnosis and clinical treatment of this disease.

Targeting the JAK/STAT Signaling Pathway for Breast Cancer.

2020 ◽  
Vol 28 ◽  
Author(s):  
Fei Shao ◽  
Xiaonan Pang ◽  
Gyeong Hun Baeg
Keyword(s):  
Breast Cancer ◽  
Signal Transduction ◽  
Signaling Pathway ◽  
Signal Transduction Pathway ◽  
Breast Cancer Treatment ◽  
Review Article ◽  
Transduction Pathway ◽  
Inhibitory Effects ◽  
Stat Proteins ◽  
Stat Signaling

Abstract:: Breast cancer is the most common malignant tumor in women worldwide. Traditional ways of treatment, includ-ing radiotherapy and endocrine therapy, for breast cancer have inevitable side effects. In recent decades, targeted therapies for breast cancer have rapidly advanced and shown a promising future. The JAK/STAT signaling pathway has been shown to play important roles in tumorigenesis, maintenance and metastasis of breast cancer. Hence, many small molecule inhibi-tors of JAK and STAT proteins have been developed. These inhibitors exhibit potent inhibitory effects on breast cancer in both cellular and animal models, and even some of them have already been in clinical trials. This review article discussed the JAK/STAT signal transduction pathway in the pathogenesis of breast cancer, and the potential for the application of JAK/STAT inhibitors in breast cancer treatment.

Identification of key mRNAs and lncRNAs involved in the effects of anti-TWEAK on Osteosarcoma

2020 ◽  
Vol 15 ◽  
Author(s):  
Mingxuan Yang ◽  
Liangtao Zhao ◽  
Xuchang Hu ◽  
Haijun Feng ◽  
Xuewen Kang
Keyword(s):  
Dna Replication ◽  
Signaling Pathway ◽  
Bioinformatics Analysis ◽  
Mapk Signaling ◽  
Migration And Invasion ◽  
Type I ◽  
Interferon Signaling ◽  
Nf Kappa B ◽  
Ppi Networks ◽  
Coexpression Networks

Background: Osteosarcoma (OS) is one of the most common primary malignant bone tumors in teenagers. Emerging studies demonstrated TWEAK and Fn14 were involved in regulating cancer cell differentiation, proliferation, apoptosis, migration and invasion. Objective: The present study identified differently expressed mRNAs and lncRNAs after anti-TWEAK treatment in OS cells using GSE41828. Methods: We identified 922 up-regulated mRNAs, 863 downregulated mRNAs, 29 up-regulated lncRNAs, and 58 down-regulated lncRNAs after anti-TWEAK treatment in OS cells. By constructing PPI networks, we identified several key proteins involved in anti-TWEAK treatment in OS cells, including MYC, IL6, CD44, ITGAM, STAT1, CCL5, FN1, PTEN, SPP1, TOP2A, and NCAM1. By constructing lncRNAs coexpression networks, we identified several key lncRNAs, including LINC00623, LINC00944, PSMB8-AS1, LOC101929787. Result: Bioinformatics analysis revealed DEGs after anti-TWEAK treatment in OS were involved in regulating type I interferon signaling pathway, immune response related pathways, telomere organization, chromatin silencing at rDNA, and DNA replication. Bioinformatics analysis revealed differently expressed lncRNAs after antiTWEAK treatment in OS were related to telomere organization, protein heterotetramerization, DNA replication, response to hypoxia, TNF signaling pathway, PI3K-Akt signaling pathway, Focal adhesion, Apoptosis, NF-kappa B signaling pathway, MAPK signaling pathway, FoxO signaling pathway. Conclusion: : This study provided useful information for understanding the mechanisms of TWEAK underlying OS progression and identifying novel therapeutic markers for OS.

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