Epigenetic alterations of the Wnt signaling pathway in cancer: a mini review

Šerman, Ljiljana; Martić, Tamara Nikuševa; Šerman, Alan; Vranić, Semir

doi:10.17305/bjbms.2014.4.205

Cited by 42 publications

(28 citation statements)

References 34 publications

(38 reference statements)

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“…Deregulated Wnt/ β -catenin signaling with cancers has been well documented in tumor initiation, progression, and metastasis, including lung cancer [18–20, 51, 52]. Blocking β -catenin signaling for cancer treatment has thus generated significant interests [53].…”

Section: Discussionmentioning

confidence: 99%

Circular RNA-ITCH Suppresses Lung Cancer Proliferation via Inhibiting the Wnt/β-Catenin Pathway

Wan

Zhang

Fan

et al. 2016

BioMed Research International

290

263

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As a special form of noncoding RNAs, circular RNAs (circRNAs) played important roles in regulating cancer progression mainly by functioning as miRNA sponge. While the function of circular RNA-ITCH (cir-ITCH) in lung cancer is still less reported, in this study, we firstly detected the expression of cir-ITCH in tumor tissues and paired adjacent noncancer tissues of 78 patients with lung cancer using a TaqMan-based quantitative real-time PCR (qRT-PCR). The results showed that the expression of cir-ITCH was significantly decreased in lung cancer tissues. In cellular studies, cir-ITCH was also enhanced in different lung cancer cell lines, A549 and NIC-H460. Ectopic expression of cir-ITCH markedly elevated its parental cancer-suppressive gene, ITCH, expression and inhibited proliferation of lung cancer cells. Molecular analysis further revealed that cir-ITCH acted as sponge of oncogenic miR-7 and miR-214 to enhance ITCH expression and thus suppressed the activation of Wnt/β-catenin signaling. Altogether, our results suggested that cir-ITCH may play an inhibitory role in lung cancer progression by enhancing its parental gene, ITCH, expression.

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Section: Discussionmentioning

confidence: 99%

Circular RNA-ITCH Suppresses Lung Cancer Proliferation via Inhibiting the Wnt/β-Catenin Pathway

Wan

Zhang

Fan

et al. 2016

BioMed Research International

290

263

View full text Add to dashboard Cite

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“…Cancer cell invasion leading to metastasis is also evident in the case of class 1 HDACs, since these are responsible for regulating E-cadherin, where the loss of E-cadherin results in the loss of cell adhesion, ultimately influencing metastasis progression [129]. Epigenetic inactivation of the inhibitors of the Wnt/β-catenin signaling cascade has also been reported to contribute to tumor metastasis [130]. In addition, studies on human cancer have shown that the hypermethylation of the promoters of Wnt antagonists, such as SFRP and DKK3, contribute to their dysregulation [131,132].…”

Section: Epigenetic Contributionmentioning

confidence: 99%

Cancer metastasis - tricks of the trade

Zeeshan

Mutahir

2017

Bosn J of Basic Med Sci

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Decades of cancer research have unraveled genetic, epigenetic and molecular pathways leading to plausible therapeutic targets; many of which hold great promise in improving clinical outcomes. Metastatic tumors become evident early on and are one of the major causes of cancer-related fatalities worldwide. This review depicts the sequential events of cancer metastasis. Genetic and epigenetic heterogeneity influences local tumor cell invasion, intravasation, survival in circulation, extravasation and colonization to distant sites. Each sequential event is associated with heterogeneous tumor microenvironment, gain of competence, unique population of cancer stem cells (CSCs), circulatory pathway, compatible niche and immune system support. A tight regulation of metastasis-promoting mechanisms and, in parallel, evading inhibitory mechanisms contribute to the severity and site of metastasis. A comprehensive understanding of tumor cell fate as an individual entity, as well as in combination with different promoting factors and associated molecular mechanisms, is anticipated in the coming years. This will enable scientists to depict design strategies for targeted cancer therapies.

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“…The GO term enrichment analysis and pathway analysis were carried out on the differentially expressed genes mentioned above, and we found that siRNA‐mediated knockdown of dbpA might regulate the expressions of tumor‐related genes through altering the biology process of SW620 cells such as signal transduction (Shimizu and Nakagawa, ), transport (Cautain et al, ), cell development (Akhtar Ali et al, ), response to stress (Pettersen et al, ), and regulation of apoptosis (Moon et al, ), which have been reported to participate in numerous types of tumors development. KEGG pathway analysis further identified that eight KEGG pathways “MAPK signaling pathway” (Lei et al, ), “Pathways in cancer” (Hein et al, ), “Chemokine signaling pathway” (Chow and Luster, ), “NOD like receptor signaling pathway” (Zaki et al, ), “Focal adhesion” (Lee et al, ) “Basal cell carcinoma” (So et al, ), and “Wnt signaling pathway” (Serman et al, ) related to tumorigenesis were significantly changed in siRNA‐dbpA group, which might be implied by that dbpA played an import role in CRC development.…”

Section: Discussionmentioning

confidence: 99%

Gene expression profile analysis of dbpA knockdown in colorectal cancer cells

Liu

Wang

Liu

et al. 2016

Cell Biology International

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DNA-binding protein A (dbpA) has been reported associated with the pathogenesis and development of various cancers. However, no evidence showed the gene expression profiling alternation involved in dbpA knockdown in colorectal cancer (CRC) cells. Small interference RNA (siRNA) method was used to knock down dbpA expression in SW620 cells. The changes of gene expression profiles in dbpA knockdown SW620 cells were determined by microarray analysis and Western blot. A total of 578 genes expressed differentially (twofold change), 181 genes were up-regulated, and 397 down-regulated in the dbpA knockdown group in comparison with the control group. The discrimination reliability was further verified by principal component analysis and Pearson correlation. Gene ontology (GO) pathway analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that the most significantly expressed genes were linked to MAPK signaling pathway. Furthermore, Western blot verified that dbpA knockdown directly inhibited the activations of TAK1, p38, and JNK in CRC cells. In conclusion, dbpA knockdown in SW620 cells altered the expression of carcinogenesis-associated genes in CRC and the involvement of dbpA on CRC might through MAPK signaling pathway, which might provide valuable evidence to further investigate the correlation between dbpA expression and CRC development.

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Epigenetic alterations of the Wnt signaling pathway in cancer: a mini review

Cited by 42 publications

References 34 publications

Circular RNA-ITCH Suppresses Lung Cancer Proliferation via Inhibiting the Wnt/β-Catenin Pathway

Circular RNA-ITCH Suppresses Lung Cancer Proliferation via Inhibiting the Wnt/β-Catenin Pathway

Cancer metastasis - tricks of the trade

Gene expression profile analysis of dbpA knockdown in colorectal cancer cells

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