Abstract
: 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 ERK2and 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 JB6C141 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.
Highlights
Colorectal cancer (CRC) is the third malignant tumor in human according to a previous epidemiological survey data [1]
The results showed that Serine/threonine kinase 33 (STK33) was overexpressed in human colorectal carcinoma HCT15, HCT116, HCT8, and DLD1 cells
The results showed that STK33 was highly expressed in 50 (84.74%) of the 59 colorectal cancerous tissues but in only 16 (27.12%) of the 59 matching normal colorectal tissues (Figure 1B, table)
Summary
Colorectal cancer (CRC) is the third malignant tumor in human according to a previous epidemiological survey data [1]. It is one of the main causes of cancer-associated mortality in the world. Further investigations are required to gain an improved understanding of the molecular characteristics and associated biological mechanisms underlying the proliferation, migration, and metastasis of CRC cells. This may enable the identification of early screening markers and therapeutic targets
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