Correlation between STK33 and the pathology and prognosis of lung cancer

Lu, Yi; Tang, Jie; Zhang, Wenmei; Chen, Shen; Xu, Ling; Yang, Danrong

doi:10.3892/ol.2017.6766

Cited by 12 publications

(9 citation statements)

References 20 publications

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“…The expression of human STKs have been reported to be frequently modulated in a variety of human cancers, and particularly, the STK35 gene is noticeably altered in human CRC ( Capra et al, 2006 ; Goyal et al, 2009 ; Lu et al, 2017 ). For the current study, we targeted STK35 based on its regulatory roles in the expression of CDKN2A, with consequent effects on the cell cycle (G1–S phase transition) and programmed cell death ( Goyal et al, 2011 ).…”

Section: Discussionmentioning

confidence: 99%

STK35 Is Ubiquitinated by NEDD4L and Promotes Glycolysis and Inhibits Apoptosis Through Regulating the AKT Signaling Pathway, Influencing Chemoresistance of Colorectal Cancer

Yang

Zhu

Wang

et al. 2020

Front. Cell Dev. Biol.

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The development of colorectal cancer (CRC) is often sporadic, but its etiology is multifactorial. Chemoresistance of CRC leads to tumor recurrence and poor prognosis in patients. The phosphorylation of protein kinase B (AKT) can activate metabolic reprogramming toward cellular glycolysis. Serine/threonine kinase 35 (STK35) regulates the cell cycle and is frequently associated with cancer progression, whereas little is known about its specific roles in CRC. In the current study, bioinformatics analyses were performed to investigate the relationship between STK35 and CRC prognosis. STK35 knockdown and overexpressing CRC cells were established to examine its functions in CRC. Fluorouracil (5-FU) was utilized to evaluate the effect of STK35 on CRC chemoresistance. Moreover, co-immunoprecipitation was performed to explore the ubiquitination of STK35. STK35 was highly expressed in CRC, and its protein expression was negatively correlated with the survival of CRC patients. Furthermore, STK35 overexpression could promote glycolysis, suppress apoptosis, upregulate p-AKT, and counteract the antitumor functions of 5-FU and neural precursor cell expressed developmentally downregulated gene 4-like (NEDD4L) in CRC cells. NEDD4L was associated with and could ubiquitinate STK35. STK35 could be a prognostic biomarker for CRC prognosis and has promotive effects on CRC cellular activities, partially through the AKT pathway. Moreover, STK35 also interferes with the chemosensitivity of CRC.

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Section: Discussionmentioning

confidence: 99%

STK35 Is Ubiquitinated by NEDD4L and Promotes Glycolysis and Inhibits Apoptosis Through Regulating the AKT Signaling Pathway, Influencing Chemoresistance of Colorectal Cancer

Yang

Zhu

Wang

et al. 2020

Front. Cell Dev. Biol.

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“…STK33 is a novel serine/threonine kinase that has been the focus of cancer studies in recent years. Previous studies have demonstrated that STK33 is overexpressed in hypopharyngeal squamous cell carcinoma [20], hepatocellular carcinoma [21], human lung cancer [16,22,23], and pancreatic cancer [18] and the increased expression of STK33 may subsequently promote tumorigenesis and disease progression. Furthermore, Yin et al studies indicated that STK33 was hypermethylated in CRC cell lines and promoted the proliferation of CRC cells [24].…”

Section: Discussionmentioning

confidence: 99%

STK33/ERK2 signal pathway contribute the tumorigenesis of colorectal cancer HCT15 cells

Zhang

Wang

et al. 2019

Bioscience Reports

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Serine/threonine kinase 33 (STK33) is a serine/threonine kinase and participates in many apoptotic process. Herein, we found that the extracellular signal-regulated kinase 2 (ERK2) was a substrate of STK33. STK33 phosphorylated ERK2 and increased the activity of ERK2 and promote the tumorigenesis of colorectal cancer HCT15 cells. Clinical simple showed that STK33 was highly expression in colorectal cells and tissues. Ex vivo and in vivo studies demonstrated that STK33 accelerate tumorigenic properties in NCM460 cells and athymic nude rats. In vitro kinase assay results indicated that STK33 can phosphorylate ERK2. Ex vivo studies further showed that STK33 can bind with ERK2 and take part in the regulation of ERKs signaling pathway. In short, our results showed that STK33 is a novel upstream kinase of ERK2. It may provide a better prospect for STK33 based prevention and treatment for colorectal cancer patients.

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“…STK33, belonging to the Ca 2+ /calmodulin dependent kinases family, plays a key role in numerous cellular functions in the range of the regulation of DNA replication, signal transduction, cell proliferation, cell differentiation, apoptosis, and tumor development 156 . STK33 has been upregulated in many types of cancers 157 .…”

Section: Signal Transduction Pathwaysmentioning

confidence: 99%

“…98 7.2 | Ca 2+ /calmodulin dependent kinase mediated pathway STK33, belonging to the Ca 2+ /calmodulin dependent kinases family, plays a key role in numerous cellular functions in the range of the regulation of DNA replication, signal transduction, cell proliferation, cell differentiation, apoptosis, and tumor development. 156 STK33 has been upregulated in many types of cancers. 157 However, the mechanism by which STK33 results in neoplasm transformation is not well understood.…”

Section: The Ras/raf/mapk Pathway and Pi3k/akt/mtor Pathwaymentioning

confidence: 99%

Recent developments in targeting genes and pathways by RNAi‐based approaches in colorectal cancer

Jebelli

Baradaran

Mosafer

et al. 2020

Medicinal Research Reviews

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A wide spectrum of genetic and epigenetic variations together with environmental factors has made colorectal cancer (CRC), which involves the colon and rectum, a challenging and heterogeneous cancer. CRC cannot be effectively overcomed by common conventional therapies including surgery, chemotherapy, targeted therapy, and hormone replacement which highlights the need for a rational design of novel anticancer therapy. Accumulating evidence indicates that RNA interference (RNAi) could be an important avenue to generate great therapeutic efficacy for CRC by targeting genes that are responsible for the viability, cell cycle, proliferation, apoptosis, differentiation, metastasis, and invasion of CRC cells. In this review, we underline the documented benefits of small interfering RNAs and short hairpin RNAs to target genes and signaling pathways related to CRC tumorigenesis. We address the synergistic effects of RNAi‐mediated gene knockdown and inhibitors/chemotherapy agents to increase the sensitivity of CRC cells to common therapies. Finally, this review points new delivery systems/materials for improving the cellular uptake efficiency and reducing off‐target effects of RNAi.

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Correlation between STK33 and the pathology and prognosis of lung cancer

Cited by 12 publications

References 20 publications

STK35 Is Ubiquitinated by NEDD4L and Promotes Glycolysis and Inhibits Apoptosis Through Regulating the AKT Signaling Pathway, Influencing Chemoresistance of Colorectal Cancer

STK35 Is Ubiquitinated by NEDD4L and Promotes Glycolysis and Inhibits Apoptosis Through Regulating the AKT Signaling Pathway, Influencing Chemoresistance of Colorectal Cancer

STK33/ERK2 signal pathway contribute the tumorigenesis of colorectal cancer HCT15 cells

Recent developments in targeting genes and pathways by RNAi‐based approaches in colorectal cancer

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