Sterol regulatory element-binding protein 1 cooperates with c-Myc to promote epithelial-mesenchymal transition in colorectal cancer

Zhai, Duanyang; Cui, Chunhui; Xie, Lang; Cai, L; Yu, Jinlong

doi:10.3892/ol.2018.8058

Cited by 16 publications

(16 citation statements)

References 24 publications

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“…Interestingly, other studies have reported that E‐cadherin suppression by the SNAIL/HDAC1/2 complex regulates metastasis in pancreatic cancer (PC) [73] and CRC [74], consistent with the hypothesis proposed in the BC study. Another study revealed that miR‐18a inhibits the proliferation of adult pancreatic progenitor cells by suppressing the activity of the proliferation‐related PI3K/AKT and ERK signaling pathways [75].…”

Section: Main Textsupporting

confidence: 86%

The dual functional role of MicroRNA‐18a (miR‐18a) in cancer development

Shen

Cao

Zhu

et al. 2019

Clinical & Translational Med

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The polycistronic miR‐17‐92 cluster is instrumental in physiological processes commonly dysregulated in cancer, such as proliferation, the cell cycle, apoptosis, and differentiation. MicroRNA‐18a (miR‐18a) is one of the most conserved and multifunctional miRNAs in the cluster and is frequently overexpressed in malignant tumors. Altered miR‐18a expression has been found in various physiological and pathological processes, including cell proliferation, apoptosis, epithelial–mesenchymal transition (EMT), tumorigenesis, cancer invasion and metastasis. In this review, we summarized the molecular basis and regulatory targets of miR‐18a in cancer development. Interestingly, miR‐18a has a dual functional role in either promoting or inhibiting oncogenesis in different human cancers. The differential miRNA expression in cancers of the same organ at different stages or of various subtypes suggests that this dual function of miR‐18a is independent of cancer type and may be attributed to the fundamental differences in tumorigenic mechanisms. Finally, we summarized the current clinical use of miR‐18a and discussed its potential uses in cancer therapy.

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Section: Main Textsupporting

confidence: 86%

The dual functional role of MicroRNA‐18a (miR‐18a) in cancer development

Shen

Cao

Zhu

et al. 2019

Clinical & Translational Med

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“…Furthermore, the same group showed that MYC directly binds the promoter of SNAIL [ 172 ]. Recently, it has been reported that the SREBP1 transcription factor facilitates the binding of MYC to the SNAIL promoter in colorectal cancer cells, thereby accelerating SNAIL expression, EMT, and migration [ 173 ]. SNAIL is named the master regulator of EMT because it exerts different functions in the process.…”

Section: Myc–the Regulator Of Emt and Metastasismentioning

confidence: 99%

MYC as a Multifaceted Regulator of Tumor Microenvironment Leading to Metastasis

Meškytė

Keskas

Ciribilli

2020

IJMS

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The Myc family of oncogenes is deregulated in many types of cancer, and their over-expression is often correlated with poor prognosis. The Myc family members are transcription factors that can coordinate the expression of thousands of genes. Among them, c-Myc (MYC) is the gene most strongly associated with cancer, and it is the focus of this review. It regulates the expression of genes involved in cell proliferation, growth, differentiation, self-renewal, survival, metabolism, protein synthesis, and apoptosis. More recently, novel studies have shown that MYC plays a role not only in tumor initiation and growth but also has a broader spectrum of functions in tumor progression. MYC contributes to angiogenesis, immune evasion, invasion, and migration, which all lead to distant metastasis. Moreover, MYC is able to promote tumor growth and aggressiveness by recruiting stromal and tumor-infiltrating cells. In this review, we will dissect all of these novel functions and their involvement in the crosstalk between tumor and host, which have demonstrated that MYC is undoubtedly the master regulator of the tumor microenvironment. In sum, a better understanding of MYC’s role in the tumor microenvironment and metastasis development is crucial in proposing novel and effective cancer treatment strategies.

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“…The epithelial–mesenchymal transition (EMT) is a biological process through which epithelial cells lose their polarity and become mesenchymal cells, gaining migratory properties that increase invasiveness in cancer progression. 9 , 10 Growing evidence suggests that the EMT is associated with metastasis and occurs during the development of various carcinomas, including CC. 11 Numerous signaling pathways are involved in the EMT process, including the Wnt, Notch, nuclear factor-kappa B, TGF-β, and RTK/Ras.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of PKM2 suppresses tumor progression in human cervical cancer by modulating epithelial–mesenchymal transition via Wnt/β-catenin signaling

Lin

Meng

et al. 2018

CMAR

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BackgroundPyruvate kinase isozyme type M2 (PKM2) is a key glycolytic enzyme and is upregulated in multiple human malignancies. However, the role of PKM2 in human cervical cancer (CC) remains elusive. Thus, this study explored the role of PKM2 in CC by detecting its expression patterns in human CC tissues and cell lines and investigated its effects on cell proliferation and invasion.Materials and methodsQuantitative reverse transcription polymerase chain reaction (qRT-PCR), immunohistochemistry and western blotting assays were used to detect the expression of PKM2 in CC tissues and CC cells. In vitro, we overexpressed and knocked down PKM2 expression in CC cell lines and investigated the biological function and underlying mechanism of PKM2 in cervical carcinogenesis.ResultsThe results showed that PKM2 mRNA and protein were highly expressed in CC tissues and cell lines. Furthermore, increasing PKM2 expression was closely correlated with the clinical stage (P=0.001) and lymph node metastasis (P=0.023). The functional roles of PKM2 were determined using Cell Counting Kit-8, colony formation, and transwell assays. The results showed that PKM2 knockdown inhibited cell proliferation and the migratory and invasive capacities of CC cells, suppressed epithelial–mesenchymal transition (EMT), and inhibited Wnt/β-catenin signaling in vitro. However, overexpression of PKM2 led to increased proliferation and invasion activity as well as the EMT in CC cells.ConclusionTaken together, our study results revealed that PKM2 may act as a molecular target for CC treatment.

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Sterol regulatory element-binding protein 1 cooperates with c-Myc to promote epithelial-mesenchymal transition in colorectal cancer

Cited by 16 publications

References 24 publications

The dual functional role of MicroRNA‐18a (miR‐18a) in cancer development

The dual functional role of MicroRNA‐18a (miR‐18a) in cancer development

MYC as a Multifaceted Regulator of Tumor Microenvironment Leading to Metastasis

Knockdown of PKM2 suppresses tumor progression in human cervical cancer by modulating epithelial–mesenchymal transition via Wnt/β-catenin signaling

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Sterol regulatory element-binding protein 1 cooperates with c-Myc to promote epithelial-mesenchymal transition in colorectal cancer

Cited by 16 publications

References 24 publications

The dual functional role of MicroRNA‐18a (miR‐18a) in cancer development

The dual functional role of MicroRNA‐18a (miR‐18a) in cancer development

MYC as a Multifaceted Regulator of Tumor Microenvironment Leading to Metastasis

Knockdown of PKM2 suppresses tumor progression in human cervical cancer by modulating epithelial&ndash;mesenchymal transition via Wnt/&beta;-catenin signaling

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Knockdown of PKM2 suppresses tumor progression in human cervical cancer by modulating epithelial–mesenchymal transition via Wnt/β-catenin signaling