Involvement of Polo-like kinase 1 (Plk1) in quiescence regulation of cancer stem-like cells of the gastric cancer cell lines

Zhu, Lin; Xing, Sheng; Zhang, Li; Yu, Jianmin; Cheng, Lin; Yang, Wei‐Jun

doi:10.18632/oncotarget.16839

Cited by 11 publications

(7 citation statements)

References 46 publications

(54 reference statements)

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“…3a ). Consistent with previous reports [ 23 , 24 ], CD44 High cells exhibited increased capacity of sphere formation compared to CD44 Low cells (Fig. 3b ).…”

Section: Resultssupporting

confidence: 93%

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Capillary morphogenesis gene 2 maintains gastric cancer stem-like cell phenotype by activating a Wnt/β-catenin pathway

Yang

et al. 2018

Oncogene

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A growing body of evidence shows that the development and progression of gastric cancer (GC) is mainly associated to the presence of gastric cancer stem-like cells (GCSLCs). However, it is unclear how GCSLC population is maintained. This study aimed to explore the role of capillary morphogenesis gene 2 (CMG2) in GCSLC maintenance and the relevance to GC progression. We found that CMG2 was highly expressed in GC tissues and the expression levels were associated with the invasion depth and lymph node metastasis of GC, and inversely correlated with the survival of GC patients. Sorted CMG2High GC cells preferentially clustered in CD44High stem-like cell population, which expressed high levels of stemness-related genes with increased capabilities of self-renewal and tumorigenicity. Depletion of CMG2 gene resulted in reduction of GCSLC population with attenuated stemness and decrease of invasive and metastatic capabilities with subdued epithelial–mesenchymal transition phenotype in GC cells. Mechanistically, CMG2 interacted with LRP6 in GCSLCs to activate a Wnt/β-catenin pathway. Thus, our results demonstrate that CMG2 promotes GC progression by maintaining GCSLCs and can serve as a new prognostic indicator and a target for human GC therapy.

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“…3a ). Consistent with previous reports [ 23 , 24 ], CD44 High cells exhibited increased capacity of sphere formation compared to CD44 Low cells (Fig. 3b ).…”

Section: Resultssupporting

confidence: 93%

“…CD44 is considered as a more reliable marker for GCSLCs as a transmembrane glycoprotein. Takaishi et al [ 23 ] and others [ 24 , 37 , 38 ] showed that CD44 High cells constitute an important GCSLC population. We found that CMG2 is preferentially expressed in CD44 High stem-like cell population.…”

Section: Discussionmentioning

confidence: 99%

Capillary morphogenesis gene 2 maintains gastric cancer stem-like cell phenotype by activating a Wnt/β-catenin pathway

Yang

et al. 2018

Oncogene

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“…The expression of MAP9 is downregulated in colorectal cancer, whereas AURKA and Plk1 are upregulated (Rouquier et al, 2014). Dysregulation of AURKA and Plk1 are strongly associated with tumorigenesis (Weng Ng et al, 2016;Al-Khafaji et al, 2017;Chen et al, 2017;Zhu et al, 2017), and AURKA polymorphisms have also been reported in association with GC and breast cancer (Lopez-Cortes et al, 2018;Mesic et al, 2017). Considering the direct interactions of MAP9 with AURKA and Plk1, we believe that MAP9 plays key role in carcinogenesis.…”

Section: Discussionmentioning

confidence: 85%

MAP9 single nucleotide polymorphism rs1058992 is a risk of EBV-associated gastric carcinoma in Chinese population

Liu¹,

Xiao²,

Wu³

et al. 2018

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Microtubule-associated protein 9 (MAP9) is a mitosis-associated protein involved in bipolar spindle assembly. Following DNA damage, MAP9 stabilizes p53 via p300 and MDM2 (mouse double minute-2 homolog). The dysregulation of MAP9 was considered to be associated with tumorigenesis. Single nucleotide polymorphisms (SNPs) in key genes governing mitosis may particularly increase susceptibility to gastric carcinoma (GC). Our study demonstrated that the CC homozygous genotype of SNP rs1058992 located in the MAP9 gene was significantly correlated with EBV-associated GC (EBVaGC) in a recessive genetic model (OR = 2.558, 95% CI = 1.306-5.010, P = 0.043), and the C allele frequency of rs1058992 also showed significant correlation with EBVaGC (OR = 1.904, 95% CI = 1.141-3.179, P = 0.013). These results suggest that the MAP9 rs1058992 polymorphism is associated with risk of EBVaGC. The conversion of lysine to arginine caused by rs1058992 may affect development of EBVaGC; however, further studies in larger populations are needed to fully elucidate its role in EBVaGC.

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“…injury or tumor acidification) and cell-intrinsic regulatory mechanisms [1,2]. Scientific literature to date supports the existence of quiescent cancer cells in many tumor types, including breast, liver and pancreatic cancer, acute myeloid leukaemia, melanoma, and glioblastoma [3,4]. In earlier studies, cells were induced to quiescence via serum starvation (whereby cells at low density were grown in serum-free medium) or contact inhibition (cells were grown in 10% serum until complete confluence) [5][6][7].…”

Section: Quiescent Tumor Cells Represent a Clinical Problemmentioning

confidence: 99%

Research progress on therapeutic targeting of quiescent cancer cells

Zhang

Gan

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Cellular quiescence (G0) is a sleep-like cellular state that allows cells to maintain the ability to re-enter and exit the proliferative cycle. Quiescent cancer cells are considered a therapeutic challenge since they are often resistant to conventional chemoradiotherapy resulting in disease progression and relapse. To date, the majority of published studies have focused on identifying molecules that target proliferating tumor cells while limited information is available on methods to target quiescent cancer cells. This review provides a summary of the relevant molecular mechanisms underlying quiescence maintenance and pharmacological interventions aimed at either eliminating this cancer cell subpopulation or indefinitely maintaining the quiescence state. Furthermore, the irradiation responses of quiescent cancer cells, in particular, the influence of manipulating intratumor hypoxia and radiation properties on radiosensitivity, are discussed. The main aim of this article is to provide a theoretical basis for the effective targeted killing of dormant tumor cells. ARTICLE HISTORY

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Involvement of Polo-like kinase 1 (Plk1) in quiescence regulation of cancer stem-like cells of the gastric cancer cell lines

Cited by 11 publications

References 46 publications

Capillary morphogenesis gene 2 maintains gastric cancer stem-like cell phenotype by activating a Wnt/β-catenin pathway

Capillary morphogenesis gene 2 maintains gastric cancer stem-like cell phenotype by activating a Wnt/β-catenin pathway

MAP9 single nucleotide polymorphism rs1058992 is a risk of EBV-associated gastric carcinoma in Chinese population

Research progress on therapeutic targeting of quiescent cancer cells

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