Abstract
Cancer stem cells (CSCs), which can self-renew and produce heterogeneous cancer cells, are the key factors during tumorigenesis. Transcription factors take essential effects on CSCs. However, the role of transcription factors in regulating the stemness of gastric cancer stem-like cells has not been well explored. In this investigation, it was found that transcription factor NME2 (NME/NM23 nucleoside diphosphate kinase 2) was upregulated in gastric cancer stem-like cells that sorted from the solid tumors of patients with gastric cancer and gastric cancer cell lines. NME2 could preserve the stemness of gastric cancer stem-like cells via suppressing their apoptosis. In vitro and in vivo data revealed that NME2 was crucial for maintaining the stemness of gastric cancer stem cells by enhancing the expression of anti-apoptosis genes. Consequently, our data contributed a new perspective to the relationship between transcription factor and the stemness maintenance of gastric cancer stem cells.
Highlights
Nowadays, gastric cancer has become the fifth highest diagnosed cancer and the third major cause of death for adults in the world [1]
The results demonstrated that the NME2 knockdown significantly increased the caspase 3/7 activity of gastric cancer stem-like cells compared with the control, while the caspase 3/7 activity of the NME2-rescue cells was comparable to that of the control (Fig. 4e)
The results showed that the percentage of tumorsphere formation of NME2-silenced cells was significantly decreased compared with the control, while the rescue of NME2 in NME2-silenced cells significantly increased the tumorsphere formation capacity (Fig. 4g)
Summary
Gastric cancer has become the fifth highest diagnosed cancer and the third major cause of death for adults in the world [1]. The interactions between environmental and host-associated factors are the main causes of high gastric cancer mortality, including the late clinical manifestations, underlying biological mechanism, and genetic heterogeneity [2]. Despite noticeable improvement in traditional treatments for gastric cancer, it is still mortal for many patients because of cancer progression, metastasis, and recurrence [3]. Due to the limitations of traditional treatment, researchers have begun to pay attention to the genetic and molecular mechanisms of tumor initiation and drug resistance [3]. Understanding CSCs may shed light on revealing the mechanisms of cancer initiation and progression, as well as the development of novel cancer therapies [4]
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