Increased expression of SRPK1 (serine/arginine-rich protein-specific kinase 1) is associated with progression and unfavorable prognosis in cervical squamous cell carcinoma

Zhanfei, Dong; Chang, Xuezhi; Xie, Li; Wang, Yina; Hou, Youxiang

doi:10.1080/21655979.2022.2034705

Cited by 7 publications

(4 citation statements)

References 50 publications

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“…Additionally, SRPK1 has been found to play an important role in the growth, metastasis, and transformation of tumors [28,29]. It is closely associated with the occurrence of various tumors, including but not limited to breast cancer [30,31], colorectal cancer [32], lung cancer [33], and cervical cancer [34]. Therefore, the function of the SRPK1 gene is not only important in normal cellular physiological processes but also significant in the occurrence and development of tumors.…”

Section: Discussionmentioning

confidence: 99%

SRPK1 Promotes Glioma Proliferation, Migration, and Invasion through Activation of Wnt/β-Catenin and JAK-2/STAT-3 Signaling Pathways

Shi,

Sun,

Deng

et al. 2024

Biomedicines

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Currently, the treatment of gliomas still relies primarily on surgery and radiochemotherapy. Although there are various drugs available, including temozolomide, the overall therapeutic effect is unsatisfactory, and the prognosis remains poor. Therefore, the in-depth study of the mechanism of glioma development and a search for new therapeutic targets are the keys to improving the therapeutic treatment of gliomas and improving the prognosis of patients. Immunohistochemistry is used to detect the expression of relevant molecules in tissues, qPCR and Western blot are used to detect the mRNA and protein expression of relevant molecules, CCK-8 (Cell Counting Kit-8) is used to assess cell viability and proliferation capacity, Transwell is used to evaluate cell migration and invasion ability, and RNA transcriptome sequencing is used to identify the most influential pathways. SRPK1 (SRSF protein kinase 1) is highly expressed in gliomas but is not expressed in normal tissues. Its expression is positively correlated with the grades of gliomas and negatively correlated with prognosis. SRPK1 significantly promotes the occurrence and development of gliomas. Knocking down SRPK1 leads to a significant decrease in the proliferation, migration, and invasion abilities of gliomas. Loss of SRPK1 expression induces G2/M phase arrest and mitotic catastrophe, leading to apoptosis in cells. Overexpression of SRPK1 activates the Wnt/β-catenin (wingless-int1/β-catenin) and JAK-2/STAT-3 (Janus kinase 2/signal transducer and activator of transcription 3) signaling pathways, promoting the proliferation, migration, and invasion of gliomas. Overexpression of SRPK1 rescues the reduced cell proliferation, migration, and invasion abilities caused by the silencing of β-catenin or JAK-2. A stable shRNA-LN229 cell line was constructed, and using a nude mouse model, it was found that stable knockout of SRPK1 significantly reduced the tumorigenic ability of glioma cells, as evidenced by a significant decrease in the subcutaneous tumor volume and weight in nude mice. We have demonstrated that SRPK1 is highly expressed in gliomas. Overexpression of SRPK1 activates the Wnt/β-catenin and JAK-2/STAT-3 signaling pathways, promoting the proliferation, migration, and invasion of gliomas. Silencing SRPK1-related signaling pathways may provide potential therapeutic options for glioma patients.

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Section: Discussionmentioning

confidence: 99%

SRPK1 Promotes Glioma Proliferation, Migration, and Invasion through Activation of Wnt/β-Catenin and JAK-2/STAT-3 Signaling Pathways

Shi,

Sun,

Deng

et al. 2024

Biomedicines

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“…Subsequently, colonies with greater than 50 cells were fixed with 4% formaldehyde for 15 min at 37°C and stained with crystal violet (Merck, Germany) for 10–20 min. Finally, the cell colonies were captured by cameras and counted from five random fields using ImageJ software (Bethesda, MD, USA) [ 25 , 27 ].…”

Section: Methodsmentioning

confidence: 99%

Luteolin impacts deoxyribonucleic acid repair by modulating the mitogen-activated protein kinase pathway in colorectal cancer

Song¹,

Wang³

et al. 2022

Bioengineered

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This study aimed to investigate the effects of luteolin on colorectal cancer (CRC) and explore its underlying mechanism. HCT-116 and HT-29 cells were treated with luteolin, cisplatin, or selumetinib. The cell survival, cell proliferation, apoptosis and cell cycle distribution, and DNA damage were detected using Cell Counting Kit-8, colony formation, flow cytometry, and immunofluorescence staining analysis, respectively. Western blotting was used to detect the expression of apoptosis-related, cycle-related, DNA-damage-related, and mitogen-activated protein kinase (MAPK) pathway-related proteins. Luteolin showed inhibitory effects on cellular growth by reducing cell survival and proliferation, inducing apoptosis and DNA damage, and arresting the cell cycle in a concentration-dependent manner in HCT-116 and HT-29 cells. Meanwhile, luteolin increased the expression of pro-apoptotic proteins, p-CHK1 (central to the induction of cell cycle arrest), and DNA excision repair protein and decreased anti-apoptotic proteins, G2-M phase-related proteins, and DNA repair proteins. The combination of cisplatin and luteolin significantly decreased cell survival and increased the apoptosis rate of HCT-116 and HT-29 cells compared with cisplatin alone. Bioinformatic analysis using the Comparative Toxicogenomics Database and STITCH and MalaCards databases showed that the MAPK pathway is involved in the pharmacology of luteolin. Furthermore, western blotting demonstrated that luteolin plays an inhibitory role by suppressing the MAPK signaling pathway in CRC, which is enhanced when combined with selumetinib. Luteolin can also prevent tumourigenesis in CRC in vivo. In conclusion, luteolin suppressed cell proliferation, blocked the cell cycle, and induced DNA damage and apoptosis progression in CRC cells by mediating the MAPK pathway

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“…Therefore, some studies have focused on searching for molecules that can predict patient survival. In this regard, some proteins have been proposed as prognostic biomarkers for CC, including the increased of Ki-67/MIB-1 protein levels [ 11 ], glucose-6-phosphatase catalytic subunit (G6PC) [ 12 ], and serine/arginine-rich protein-specific kinase 1 (SRPK1) [ 13 ], which are related with worse survival, while the high levels of Galectin 9 [ 14 ] correlate with a better prognosis in CC patients. Moreover, through the analysis of transcriptional profiles derived from genomic databases of CC patients, genes related to OS have been identified [ 15 , 16 ].…”

Section: Introductionmentioning

confidence: 99%

RIPOR2 Expression Decreased by HPV-16 E6 and E7 Oncoproteins: An Opportunity in the Search for Prognostic Biomarkers in Cervical Cancer

Olmedo-Nieva

Muñoz-Bello

Martínez-Ramírez

et al. 2022

Cells

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High-risk human papillomavirus (HPV) infection is the main risk factor for cervical cancer (CC) development, where the continuous expression of E6 and E7 oncoproteins maintain the malignant phenotype. In Mexico, around 70% of CC cases are diagnosed in advanced stages, impacting the survival of patients. The aim of this work was to identify biomarkers affected by HPV-16 E6 and E7 oncoproteins that impact the prognosis of CC patients. Expression profiles dependent on E6 and E7 oncoproteins, as well as their relationship with biological processes and cellular signaling pathways, were analyzed in CC cells. A comparison among expression profiles of E6- and E7-expressing cells and that from a CC cohort obtained from The Cancer Genome Atlas (TCGA) demonstrated that the expression of 13 genes impacts the overall survival (OS). A multivariate analysis revealed that the downregulated expression of RIPOR2 was strongly associated with a worse OS. RIPOR2, including its transcriptional variants, were overwhelmingly depleted in E6- and E7-expressing cells. Finally, in a Mexican cohort, it was found that in premalignant cervical lesions, RIPOR2 expression decreases as the lesions progress; meanwhile, decreased RIPOR2 expression was also associated with a worse OS in CC patients.

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Increased expression of SRPK1 (serine/arginine-rich protein-specific kinase 1) is associated with progression and unfavorable prognosis in cervical squamous cell carcinoma

Cited by 7 publications

References 50 publications

SRPK1 Promotes Glioma Proliferation, Migration, and Invasion through Activation of Wnt/β-Catenin and JAK-2/STAT-3 Signaling Pathways

SRPK1 Promotes Glioma Proliferation, Migration, and Invasion through Activation of Wnt/β-Catenin and JAK-2/STAT-3 Signaling Pathways

Luteolin impacts deoxyribonucleic acid repair by modulating the mitogen-activated protein kinase pathway in colorectal cancer

RIPOR2 Expression Decreased by HPV-16 E6 and E7 Oncoproteins: An Opportunity in the Search for Prognostic Biomarkers in Cervical Cancer

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