“…Moreover, using a web server for cancer and normal gene GEPIA, we found that PKMYT1 expression was significantly higher in ESCC tumor tissues than in normal tissues (Figure 2B). The expression of PKMYT1 associated with some important genes of ESCC, such as Ki67, TWIST,23,24 AKT (Figure 2C). 25,26Figure 2PKMYT1 associates with prognosis in several cancers and correlates with several crucial functional genes in ESCC.…”
Section: Resultsmentioning
confidence: 97%
“…This indicated that PKMYT1 might promote the EMT progression in ESCC cells. Multiple reports have demonstrated that Twist, VIM, NCAD, and ECAD were independent risk factors in ESCC and associated with ESCC patients’ prognosis 23,24,39. Thus, PKMYT1 may participate in EMT of ESCC cells via these related molecular network.…”
BackgroundEsophageal squamous cell carcinoma (ESCC) is one of the most common malignant tumors worldwide and the 5-year overall survival rate remains poor. Protein kinase, membrane associated tyrosine/threonine (PKMYT1) is overexpressed in several cancers and participate in tumor progression. However, the mechanism of PKMYT1 in ESCC is unclear.PurposeThe objective of our study was to demonstrate the the expression and role of PKMYT1 in ESCC.Patients and methods We detected the expression of PKMYT1 in ESCC patients and analysed the correlation with overall survival time and disease-free survival time. Then we detected PKMYT1 expression in ESCC cell lines and immortalized human esophageal epithelial cell line. Down-regulated PKMYT1 was carried out in KYSE70 and KYSE450 cells to invetigate the mechanism of PKMYT1 in ESCC cells.ResultsPKMYT1 was up-regulated in tumor tissues and ESCC cell lines, and higher expression of PKMYT1 correlated with poorer overall survival in ESCC patients. Besides, in ESCC cell lines KYSE70 and KYSE450, knocking down PKMYT1 allowed more cells to skip G2/M checkpoint to complete mitosis, which promoted cell apoptosis, inhibited cell proliferation, and prevented the EMT phenotype in vitro. Meantime, we also observed that down-regulated PKMYT1 in ESCC cells suppressed AKT/mTOR signaling pathway. These results demonstrated PKMYT1 may act as an oncogene in ESCC.ConclusionPKMYT1 plays an crutial role in ESCC progression, downregulated PKMYT1 might inhibit the development of ESCC by AKT/mTOR signaling pathway, and might be a novel target in the treatment of ESCC.
“…Moreover, using a web server for cancer and normal gene GEPIA, we found that PKMYT1 expression was significantly higher in ESCC tumor tissues than in normal tissues (Figure 2B). The expression of PKMYT1 associated with some important genes of ESCC, such as Ki67, TWIST,23,24 AKT (Figure 2C). 25,26Figure 2PKMYT1 associates with prognosis in several cancers and correlates with several crucial functional genes in ESCC.…”
Section: Resultsmentioning
confidence: 97%
“…This indicated that PKMYT1 might promote the EMT progression in ESCC cells. Multiple reports have demonstrated that Twist, VIM, NCAD, and ECAD were independent risk factors in ESCC and associated with ESCC patients’ prognosis 23,24,39. Thus, PKMYT1 may participate in EMT of ESCC cells via these related molecular network.…”
BackgroundEsophageal squamous cell carcinoma (ESCC) is one of the most common malignant tumors worldwide and the 5-year overall survival rate remains poor. Protein kinase, membrane associated tyrosine/threonine (PKMYT1) is overexpressed in several cancers and participate in tumor progression. However, the mechanism of PKMYT1 in ESCC is unclear.PurposeThe objective of our study was to demonstrate the the expression and role of PKMYT1 in ESCC.Patients and methods We detected the expression of PKMYT1 in ESCC patients and analysed the correlation with overall survival time and disease-free survival time. Then we detected PKMYT1 expression in ESCC cell lines and immortalized human esophageal epithelial cell line. Down-regulated PKMYT1 was carried out in KYSE70 and KYSE450 cells to invetigate the mechanism of PKMYT1 in ESCC cells.ResultsPKMYT1 was up-regulated in tumor tissues and ESCC cell lines, and higher expression of PKMYT1 correlated with poorer overall survival in ESCC patients. Besides, in ESCC cell lines KYSE70 and KYSE450, knocking down PKMYT1 allowed more cells to skip G2/M checkpoint to complete mitosis, which promoted cell apoptosis, inhibited cell proliferation, and prevented the EMT phenotype in vitro. Meantime, we also observed that down-regulated PKMYT1 in ESCC cells suppressed AKT/mTOR signaling pathway. These results demonstrated PKMYT1 may act as an oncogene in ESCC.ConclusionPKMYT1 plays an crutial role in ESCC progression, downregulated PKMYT1 might inhibit the development of ESCC by AKT/mTOR signaling pathway, and might be a novel target in the treatment of ESCC.
“…It was revealed in this study that MEIS1 knockdown causes a significant decrease in TWIST1 gene expression in KYSE‐30 cells. TWIST1 not only involves in embryonic organogenesis, specification, and differentiation, but also is associated with tumor initiation, angiogenesis, stemness and EMT (epithelial‐mesenchymal transition) promotion, leading tumor cell invasion and metastasis in a variety of human malignancies (Forghanifard, Rad, et al, ). It has been indicated that silencing of TWIST1 lead to increase osteoblast differentiation in mesenchymal stem cells (MSCs) by upregulation of the involved genes in FGF/ERK and BMP signaling pathways (Miraoui, Severe, Vaudin, Pagès, & Marie, ).…”
Background
MEIS1
(Myeloid ecotropic viral integration site 1), as a homeobox (HOX) transcription factor, has a dual function in different types of cancer. Although numerous roles are proposed for
MEIS1
in differentiation, stem cell function, gastrointestinal development and tumorigenesis, the involved molecular mechanisms are poor understood. Our aim in this study was to elucidate the functional correlation between
MEIS1
, as regulator of differentiation process, and the involved genes in cell differentiation in human esophageal squamous carcinoma (ESC) cell line KYSE‐30.
Methods
The KYSE‐30 cells were transduced using recombinant retroviral particles containing specific shRNA sequence against
MEIS1
to knockdown
MEIS1
gene expression. Following RNA extraction and cDNA synthesis, mRNA expression of
MEIS1
and the selected genes including
TWIST1, EGF, CDX2,
and
KRT4
was examined using relative comparative real‐time PCR.
Results
Retroviral transduction caused a significant underexpression of
MEIS1
in GFP‐hMEIS1 compared to control GFP cells approximately 5.5‐fold. While knockdown of
MEIS1
expression caused a significant decrease in
EGF
and
TWIST1
mRNA expression, nearly ‐8‐ and ‐12‐fold respectively, it caused a significant increase in mRNA expression of differentiation markers including
KRT4
and
CDX2
, approximately 34‐ and 1.14‐fold, correspondingly.
Conclusion
MEIS1
gene silencing in KYSE‐30 cells increased expression of epithelial markers and decreased expression of epithelial‐mesenchymal transition (EMT) marker
TWIST1
. It may highlight the role of
MEIS1
in differentiation process of KYSE‐30 cells. These results may confirm that
MEIS1
silencing promotes differentiation and decreases EMT capability of ESC cell line KYSE‐30.
“…The overexpression of MAGE-A4 promoted the growth of spontaneously transformed normal oral keratinocytes by inhibiting apoptosis and growth arrest in the G1-phase of the cell cycle [56]. Moreover, MAGE-A4 may be a direct target of TWIST1 [58], which also up-regulates cell cycle progression, proliferation and migration and inhibits cell death in cancer and embryonic cells [59].…”
The biological roles of cancer-testis antigens of the Melanoma antigen (Mage) family in mammalian development, stem cell differentiation and carcinogenesis are largely unknown. In order to understand the involvement of the
Mage
family genes in maintenance of normal and cancer stem cells, the expression patterns of
Mage-a, Mage-b, Mage-d, Mage-e, Mage-h
and
Mage-l
gene subfamilies were analyzed during the self-renewal and differentiation of mouse pluripotent stem and teratocarcinoma cells. Clustering analysis based on the gene expression profiles of undifferentiated and differentiating cell populations revealed strong correlations between
Mage
expression patterns and differentiation and malignant states. Gene co-expression analysis disclosed the potential contributions of
Mage
family members in self-renewal and differentiation of pluripotent stem and teratocarcinoma cells. Two gene clusters including
Mage-a4
and
Mage-a8, Mageb1, Mage-d1, Mage-d2, Mage-e1, Mage-l2
were identified as functional antagonists with opposing roles in the regulation of proliferation and differentiation of mouse pluripotent stem and teratocarcinoma cells. The identified aberrant expression patterns of
Mage-a2, Mage-a6, Mage-b4, Mageb-16
and
Mage-h1
in teratocarcinoma cells can be considered as specific teratocarcinoma biomarkers promoted the malignant phenotype. Our study first provides a model for the involvement of
Mage
family members in regulatory networks during the self-renewal and early differentiation of normal and cancerous stem cells for further research of the predicted functional modules and the development of new cancer treatment strategies.
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