Expression profiles of cancer stem cell markers: CD133, CD44, Musashi-1 and EpCAM in the cardiac mucosa—Barrett’s esophagus—early esophageal adenocarcinoma—advanced esophageal adenocarcinoma sequence

Mokrowiecka, Anna; Veits, Lothar; Falkeis, Christina; Musiał, Jacek; Kordek, Radzisław; Łochowski, Mariusz; Kozak, Józef; Wierzchniewska-Ławska, Agnieszka; Małecka‐Panas, Ewa

doi:10.1016/j.prp.2016.12.018

Cited by 22 publications

(17 citation statements)

References 31 publications

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“…In the experiment of investigating the mechanism of the speci c binding, we found the receptor of binding to SNF peptide was Epithelial cell adhesion molecule (EpCAM) (20). EpCAM was observed on the cell surfaces of EAC (21), which is consistent to our observation under confocal microscopy.…”

Section: Discussionsupporting

confidence: 87%

Targeted imaging of esophageal adenocarcinoma with a near-infrared fluorescent peptide

Kang¹,

Liu

et al. 2020

Preprint

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Background: Targeted optical imaging offers a noninvasive and accurate method for the early detection of gastrointestinal tumors, especially for flat appearances. In our previous study, a sequence of SNFYMPL (SNF) was identified as a specific peptide to bind to esophageal carcinoma using phage-display technology. This study aimed to evaluate the tumor-targeting efficacy of Cy5.5-conjugated SNF probe for imaging of esophageal carcinoma in vitro and in vivo.Methods: The SNF-Cy5.5 probe was synthesized and then identified using High Performance Liquid Chromatography (HPLC) and mass spectrometry (MS). Confocal fluorescence imaging and Flow cytometry analysis were performed to evaluate the binding specificity and the receptor binding affinity of SNF-Cy5.5 to OE33. In vivo imaging was performed to evaluate the targeting ability of SNF-Cy5.5 to esophageal carcinoma.Results：The confocal imaging and flow cytometry analysis showed that SNF-Cy5.5 bound specifically to the plasma membrane of OE33 cells with a high affinity. In vivo, for non-block group, SNF-Cy5.5 probe exhibited rapid OE33 tumor targeting during 24 h p.i. and excellent tumor-to-background contrast at 2 h p.i. For the block group, SNF-Cy5.5 was not observed in the mice after 4h p.i. Ex vivo imaging also revealed that a higher fluorescent signal intensity value of the tumors was clearly observed in the non-block group than that in the block group (2.6 ± 0.32× 109 vs 0.8 ± 0.08× 109, p < 0.05).Conclusions: SNF -Cy5.5 was synthesized and characterized with a high efficiency and purity. The higher affinity, specificity, and tumor targeting efficacy of SNF-Cy5.5 were confirmed by in vitro and in vivo tests. SNF-Cy5.5 is a promising optical probe for the imaging of esophageal adenocarcinoma.

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Section: Discussionsupporting

confidence: 87%

Targeted imaging of esophageal adenocarcinoma with a near-infrared fluorescent peptide

Kang¹,

Liu

et al. 2020

Preprint

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“…Some other studies have reported higher expression of hnRNP‐B1 (Matsuyama et al, ) and ‐H1 (Sun, Liu, Liu, & Zhao, ), NF45 (Ni et al, ), insulin‐like growth factor 2 mRNA‐binding protein (IGF2BP)‐2 (Barghash, Golob‐Schwarzl, Helms, Haybaeck, & Kessler, ) and ‐3 (W. Feng et al, ; Kazeminezhad, Mirafsharieh, Dinyari, Azizi, & Ebrahimi, ; Trivedi, Cartun, & Ligato, ), DEAD‐Box Helicase 46 (B. Li, Li, et al, ), and Musashi‐1 (Mokrowiecka et al, ) in EC tissues. Because enhanced expression of these molecules was correlated with poor pathologic features and worse survival of patients, they are thought to be useful as new prognostic markers and potential anticancer targets in EC.…”

Section: Major Functions Of Rbps In Gi Cancermentioning

confidence: 97%

Diverse roles of RNA‐binding proteins in cancer traits and their implications in gastrointestinal cancers

Masuda

Kuwano

2018

WIREs RNA

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Gene expression patterns in cancer cells are strongly influenced by posttranscriptional mechanisms. RNA-binding proteins (RBPs) play key roles in posttranscriptional gene regulation; they can interact with target mRNAs in a sequence-and structure-dependent manner, and determine cellular behavior by manipulating the processing of these mRNAs. Numerous RBPs are aberrantly deregulated in many human cancers and hence, affect the functioning of mRNAs that encode proteins, implicated in carcinogenesis. Here, we summarize the key roles of RBPs in posttranscriptional gene regulation, describe RBPs disrupted in cancer, and lastly focus on RBPs that are responsible for implementing cancer traits in the digestive tract. These evidences may reveal a potential link between changes in expression/function of RBPs and malignant transformation, and a framework for new insights and potential therapeutic applications.

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“…Recent studies have shown that cancer stem cells (CSCs) or tumor-initiating cells, a rare undifferentiated fraction of tumor cells with distinct stem cell-like features, are strongly implicated with chemo- or radiation-resistance, metastasis, and high rate of tumor recurrence 1 , 2 . Several cancer stem cell markers have been suggested, such as CD44, CD133, and EpCAM, most of which are cell surface molecules and have investigated as CSC-targeting molecules 3 – 5 . Aldehyde dehydrogenase isoform 1 (ALDH1) also has been suggested as a CSC marker in various cancers 6 , 7 .…”

Section: Introductionmentioning

confidence: 99%

Tescalcin/c-Src/IGF1Rβ-mediated STAT3 activation enhances cancer stemness and radioresistant properties through ALDH1

Lee

Choi

Kim

et al. 2018

Sci Rep

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Tescalcin (TESC; also known as calcineurin B homologous protein 3, CHP3) has recently reported as a regulator of cancer progression. Here, we showed that the elevation of TESC in non-small cell lung cancer (NSCLC) intensifies epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) properties, consequently enhancing the cellular resistance to γ-radiation. TESC expression and the phosphorylation (consequent activation) of signal transducer and activator of transcription 3 (STAT3) were upregulated in CSC-like ALDH1high cells than in ALDH1low cells sorted from A549 NSCLC cells. Knockdown of TESC suppressed CSC-like properties as well as STAT3 activation through inhibition of insulin-like growth factor 1 receptor (IGF1R), a major signaling pathway of lung cancer stem cells. TESC activated IGF1R by the direct recruitment of proto-oncogene tyrosine kinase c-Src (c-Src) to IGF1Rβ complex. Treatment of IGF1R inhibitor, AG1024, also suppressed c-Src activation, implicating that TESC mediates the mutual activation of c-Src and IGF1R. STAT3 activation by TESC/c-Src/IGF1R signaling pathway subsequently upregulated ALDH1 expression, which enhanced EMT-associated CSC-like properties. Chromatin immunoprecipitation and luciferase assay demonstrated that STAT3 is a potential transcription activator of ALDH1 isozymes. Ultimately, targeting TESC can be a potential strategy to overcome therapeutic resistance in NSCLC caused by augmented EMT and self-renewal capacity.

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Expression profiles of cancer stem cell markers: CD133, CD44, Musashi-1 and EpCAM in the cardiac mucosa—Barrett’s esophagus—early esophageal adenocarcinoma—advanced esophageal adenocarcinoma sequence

Cited by 22 publications

References 31 publications

Targeted imaging of esophageal adenocarcinoma with a near-infrared fluorescent peptide

Targeted imaging of esophageal adenocarcinoma with a near-infrared fluorescent peptide

Diverse roles of RNA‐binding proteins in cancer traits and their implications in gastrointestinal cancers

Tescalcin/c-Src/IGF1Rβ-mediated STAT3 activation enhances cancer stemness and radioresistant properties through ALDH1

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