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 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 Evaluation of the Oncogene Function of GOLPH3 and Correlated Regulatory Network in Lung Adenocarcinoma

2021 ◽  
Vol 11 ◽  
Author(s):  
Tong Zhang ◽  
Yue Wang ◽  
Yangyang Chen ◽  
Shuo Jin ◽  
Ying Gao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Survival Analysis ◽  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Interaction Network ◽  
Cell Receptor ◽  
Migration And Invasion ◽  
Biological Regulation ◽  
Protein Protein Interaction ◽  
Human Protein Atlas

BackgroundGolgi phosphoprotein 3 (GOLPH3) is an oncoprotein localized in the Golgi apparatus. Abnormal GOLPH3 expression is potentially related to carcinogenesis. However, the potential biological regulation network of GOLPH3 in lung adenocarcinoma (LUAD) remains to be determined.MethodsExpression of GOLPH3 was identified in LUAD via TIMER, Oncomine, Lung Cancer Explorer (LCE), Human Protein Atlas (HPA), and UALCAN database. Survival analysis was performed using the Kaplan–Meier plotter. GOLPH3 alterations were analyzed through cBioPortal. LinkedOmics was used to perform functional analysis and predict interacted targets. The protein–protein interaction network was constructed by GeneMANIA. In addition, candidate miRNAs and lncRNAs targeting GOLPH3 were generated to construct competing endogenous RNA (ceRNA) network, and survival analysis of ceRNA was performed using LnCeVar. The mRNA or protein expression of TUG1, miR-142-5p, and GOLPH3 in Beas-2B and LUAD cells was verified using qPCR or Western blotting. CCK-8 assay, wound healing assay, and transwell assay were used to detect the ability of cell proliferation, migration, and invasion.ResultsOverexpression of GOLPH3 was identified in LUAD. UALCAN analysis showed that upregulated GOLPH3 was linked to different pathological features of LUAD patients. Importantly, high GOLPH3 expression indicated a negative correlation with the first progression (FP) in LUAD patients. GOLPH3 alterations were also found. Moreover, co-expressed genes with GOLPH3 were analyzed; and they were involved in ribosome and oxidative phosphorylation pathways. Functional network analysis indicated GOLPH3 regulated T-cell receptor signaling pathway and interferon signaling pathway with kinase and transcription factor targets. Notably, TUG1/miR-142-5p/GOLPH3 affected overall survival of LUAD patients. GOLPH3 expression was decreased in the cells with overexpression of miR-142-5p and TUG1 knockdown. GOLPH3 reduction inhibited cell proliferation, migration, and invasion.ConclusionsUpregulation of GOLPH3 has a positive correlation with clinicopathological subtypes and poor FP in LUAD. GOLPH3 promoted LUAD progression. Moreover, TUG1 may act as ceRNA to regulate GOLPH3 expression by competitive binding miR-142-5p.

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.

USF1 Promotes Lung Adenocarcinoma Progression by Regulating Neurotrophin Signaling Pathway

2021 ◽  
Author(s):  
Yu Wang ◽  
Yunxia Zhao ◽  
Xiangwei Zhang ◽  
Yuanzhu Jiang ◽  
Wei Ma ◽  
...  
Keyword(s):  
Mouse Model ◽  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Expression Level ◽  
Migration And Invasion ◽  
Cellular Viability ◽  
Invasion Potential ◽  
Clinical Records ◽  
Neurotrophin Signaling ◽  
Related Proteins

Abstract Background: We aimed at investigation of the effect and the underlying neurotrophin signaling pathway of the upstream transcription factor 1 (USF1) in lung adenocarcinoma (LUAD).Methods: The Cancer Genome Atlas (TCGA) database was used to analyze USF1 expression data and to extract patients’ clinical records. Immunohistochemical assay and Western blotting (WB) were used to determine the expression levels of USF1 in LUAD. The neurotrophin signaling pathway was analyzed by bioinformatic analysis while the expression of all related proteins was determined by WB. In addition cellular viability, proliferation, migration and invasion potential were investigated by the CCK-8, colony formation, wound healing and transwell. Meanwhile, the effect of USF1 in LUAD progression was investigated in a mouse model. The link between USF1 and UGT1A3 (UDP Glucuronosyltransferase Family 1 Member A3) was studied by the dual-luciferase reporter assay. Results: We have detected a high expression level of USF1 in LUAD, which was associated with advanced tumor stage, nodal metastasis, and poor patient’s survival rate. The knockdown of USF1 inhibited cellular viability, proliferation, migration and invasion. Meanwhile, USF1 knockdown inhibited tumor growth in a mouse model. Besides, USF1 targeted UGT1A3, which was proven by the fact that the USF1 knockdown decreased the expression level of UGT1A3, whereas the upregulated expression of UGT1A3 increased cellular viability and proliferation. We have proved that the neurotrophin signaling pathway in LUAD was activated by USF1 and UGT1A3. The expression of the related proteins was also inhibited by the USF1 knockdown, while the overexpression of IRAK increased cancer cells’ migration and invasion potential.Conclusion: USF1 was highly expressed in LUAD and promoted LUAD progression by regulating the neurotrophin signaling pathway. These findings provide a new theoretical data that could serve as a good foundation for the treatment of LUAD.

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

MiR-186 serves as a tumor suppressor in lung adenocarcinoma cells by down-regulation of Shp2 gene and inhibiting PI3K/Akt/mTOR signaling pathway

2020 ◽  
Author(s):  
Shao-Hui Yan ◽  
Shu-Feng Xu ◽  
Lei Zheng ◽  
Li-Ying Kang ◽  
Jun-Li Cao ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Tyrosine Phosphatase ◽  
Negative Control ◽  
Mtor Signaling ◽  
Migration And Invasion ◽  
Mtor Signaling Pathway ◽  
Blank Group ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells

Abstract Background The study aimed to investigate the effect and mechanism of miR-186, which targets protein tyrosine phosphatase (Shp2) PI3K/Akt/mTOR signaling pathway, on the biological characteristics of lung adenocarcinoma cells. Methods In this experimental study, Human lung adenocarcinoma cell line SPC-A-1 was grouped as Blank group, negative control (NC) group, miR-186 mimic group, miR-186 inhibitor group, si-Shp2 group and miR-186 inhibitor+si-Shp2 group. Results The results showed that miR-186 can target and down-regulate the expression of Shp2 gene. Compared with the Blank group, levels of Shp2, N-cadherin and Bcl-2 and level of PI3K/p-PI3K, Akt/P-Akt, mTOR/p-mTOR as well as cell proliferation, migration and invasion ability and the proportion of cells in S phase significantly decreased in the miR-186 mimic group and the si-Shp2 group, while the levels of E-cadherin and Bax as well as the proportion of cells in G1 phase and cell gene and mediates apoptosis rate increased significantly (all P < 0.05). Compared with the miR-186 inhibitor group, the miR-186 inhibitor + si-Shp2 group showed similar trend in all parameters with the comparison above (all P < 0.05). Conclusions The overexpression of miR-186 can down-regulate Shp2 gene expression, further inhibit the proliferation, invasion and migration and promote apoptosis of lung adenocarcinoma cells by inhibiting the activation of PI3K/Akt/mTOR signaling pathway.

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