The roles of Wnt/β-catenin signaling pathway related lncRNAs in cancer

Hu, Xiaofan; Hou, Pingfu; Li, Teng-Teng; Quan, Haoyu; Li, Min-Le; Lin, Tian; Liu, Jin-Jin; Bai, Jing; Zheng, Junnian

doi:10.7150/ijbs.27977

Cited by 61 publications

(36 citation statements)

References 133 publications

(110 reference statements)

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“…Still worth of mention that according to the previous studies, WNT signaling might be responsible for checkpoint inhibitor resistance and immunological difficulties in treating colorectal cancer [48][49][50]. As it appear in our study, lncRNA in canonical WNT signaling in colorectal cancer also has a significant role in the transition from stage-1 to stage-4; this notion additionally has been proven by experimental works [43,51]. HOTAIR is one of these LNCs that could contribute to the overexpression of WNT signaling [52].…”

Section: Discussionsupporting

confidence: 80%

A comprehensive investigation of colorectal cancer progression, from the early to late-stage, a systems biology approach

Ghorbani

Asgari

2020

Preprint

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Colorectal cancer is a widespread malignancy with a concerning mortality rate. It could be curable at the first stages, but the progress of the disease and reaching to the stage-4 could make shift the treatments from curative to palliative. In this stage, the survival rate is meager, and therapy options are limited. The question is, what are the hallmarks of this stage and what genes are involved? What mechanism and pathways could drive such a malign shift from stage-1 to stage-4? In this study, first we identified the core modules for both the stage-1 and stage-4 which four of them have a significant role in stage-1 and two of them have a role in stage-4. Then we investigated the gene ontology and hallmarks analysis for each stage. According to the results, the immune-related process, especially interferon-gamma, impacts stage-1 in colorectal cancer. Concerning stage-4, extracellular matrix ontologies, and metastatic hallmarks are in charge. At last, we performed a differentially expressed gene analysis of stage-4 vs. stage-1 and analyzed their pathways which reasonably undergone a hypo/hyperactivity or being abnormally regulated through the cancer progression. We found that lncRNA in canonical WNT signaling and colon cancer has the most significant pathways, followed by WNT signaling, which means that these pathways may be the driver for the development from early-stage to late-stage. Of these lncRNAs, we had two upregulated kind, H19, and HOTAIR, which both can be involved and mediate metastasis and invasion in colorectal cancer.

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Section: Discussionsupporting

confidence: 80%

A comprehensive investigation of colorectal cancer progression, from the early to late-stage, a systems biology approach

Ghorbani

Asgari

2020

Preprint

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“…In the absence of activated Wnt signalling, b-catenin is actively degraded to maintain a low level of b-catenin in the cytosol. However, when canonical Wnt signalling is activated, b-catenin accumulates in the cytosol and migrates to the nucleus, where it interacts with the T-cell factor/lymphocyte enhancer factor and co-activators to stimulate the transcription of the downstream target genes, such as c-Myc, cyclin D1, thus promoting uncontrolled cell proliferation [38,39]. It was demonstrated that XAV939 could suppress cell growth and proliferation in neuroblastoma cell lines through the inhibition of TNKS1 [37].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Wnt signalling pathway by XAV939 enhances radiosensitivity in human cervical cancer HeLa cells

Zhang

Gan

et al. 2020

Artificial Cells, Nanomedicine, and Biotechnology

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Cervical cancer is the second most common malignant tumour threatening women's health. In recent years, heavy-ion beam therapy is becoming a newly emerging therapeutic mean of cancer; however, radio-resistance and radiation-induced damage constitute the main obstacles for curative treatment of cervical cancer. Therefore, to identify the radiosensitizers is essential. Here, we investigated the effects of Wnt signalling pathway on the response of 12 C 6þ radiation in HeLa cells. XAV939, an inhibitor of Wnt signalling pathway, was added two hours before 12 C 6þ radiation. 12 C 6þ radiation inhibited the viability of HeLa cells in a time-dependent manner, and inhibiting Wnt signalling using XAV939 significantly intensified this stress. Meanwhile, 12 C 6þ radiation induced a significant increased cell apoptosis, G2/M phase arrest, and the number of c-H2AX foci. Supplementation with XAV939 significantly increased the effects induced by 12 C 6þ radiation alone. Combining XAV939 with 12 C 6þ irradiation, the expression of apoptotic genes (p53, Bax, Bcl-2) was significantly increased, while the expression of Wnt-related genes (Wnt3a, Wnt5a, b-catenin, cyclin D1 and c-Myc) was significantly decreased. Overall, these findings suggested that blockage of the Wnt/b-catenin pathway effectively sensitizes HeLa cells to 12 C 6þ irradiation, and it may be a potential therapeutic approach in terms of increasing the clinical efficacy of 12 C 6þ beams.

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“… 10 Growing evidence has also indicated that Wnt/β-catenin signaling components are regulated by not only long non-coding RNAs (lncRNAs) but also other noncoding classes. 11 12 13 14 15 …”

Section: Introductionmentioning

confidence: 99%

LUCAT1 Epigenetically Downregulates the Tumor Suppressor Genes CXXC4 and SFRP2 in Gastric Cancer

2020

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Purpose The mechanisms of Wnt/β-catenin pathway signaling and abnormal expression of tumor suppressor genes is not well known in gastric cancer (GC). Long non-coding RNA (lncRNA) has recently been identified as a possible link therein. In this study, we investigated the role of lung cancer associated transcript 1 (LUCAT1) in GC. Materials and Methods The expression of LUCAT1 in GC cell lines and 100 tissue samples was examined by qRT-PCR. Two different siRNAs were used for knockdown of LUCAT1 expression. Cell viability was assessed by MTT assay. To analyze metastasis, scratch wound-healing assay, a Matrigel invasion assay, and colony formation assay were performed. Apoptosis was analyzed by PI/Annexin-V staining. To check the methylation status in tumor suppressor genes, methylation-specific PCR was carried out. Western blot was performed to detect epithelial-mesenchymal transition and apoptosis markers upon silencing of LUCAT1 (siLUCAT1). Results LUCAT1 expression in GC cell lines and tissues was significantly elevated, compared to that in normal gastric cells and adjacent non-tumor tissues ( p <0.001). Two different siRNAs for LUCAT1 reduced cell proliferation, invasion, and migration, compared to siCT ( p <0.05), and these reductions were restored by pcDNA-LUCAT1 ( p <0.05). siLUCAT1 elicited upregulation of the expression of CXXC4 and SFRP2 . The expression of H3K27me3 was reduced by siLUCAT1, and this reduction was correlated with methylation of CXXC4 and SFRP2 . Inhibition of LUCAT1 up-regulated EZH2 expression and resulted in demethylation of CXXC4 and SFRP2 through the Wnt/β-catenin signaling pathway. Conclusion We concluded that LUCAT1 induces methylation of CXXC4 and SFRP2 , thereby regulating Wnt/β-catenin signaling in GC.

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The roles of Wnt/β-catenin signaling pathway related lncRNAs in cancer

Cited by 61 publications

References 133 publications

A comprehensive investigation of colorectal cancer progression, from the early to late-stage, a systems biology approach

A comprehensive investigation of colorectal cancer progression, from the early to late-stage, a systems biology approach

Inhibition of Wnt signalling pathway by XAV939 enhances radiosensitivity in human cervical cancer HeLa cells

LUCAT1 Epigenetically Downregulates the Tumor Suppressor Genes CXXC4 and SFRP2 in Gastric Cancer

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