Transcriptional Regulation of Wnt/β-Catenin Pathway in Colorectal Cancer

Ji, Bing; Dannappel, Marius; Wan, Chunhua; Firestein, Ron

doi:10.3390/cells9092125

Cited by 165 publications

(130 citation statements)

References 258 publications

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“…The canonical Wnt signaling pathway participates in normal functioning of diverse physiological processes. However, its abnormal aberrant activation results in the development and progression of cancer 17 , 40 , 50 , 51 . We identified miR23a-5p binding sites on Wnt3a using the RNA hybrid database and showed reduced luciferase activity on HB cell lines co-transfected with Wnt3aWT and miR-23a-mimics.…”

Section: Discussionmentioning

confidence: 99%

SNHG9 promotes Hepatoblastoma Tumorigenesis via miR-23a-5p/Wnt3a Axis

Feng¹,

Bhandari²,

Liu³

et al. 2021

J. Cancer

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Background: Hepatoblastoma is a common hepatic tumor occurring in children between 0-5 years. Accumulating studies have shown lncRNA's potential role in distinct cancer progression and development, including hepatoblastoma. SnoRNA host gene 9 (SNHG9) is associated with the progression of distinct human cancers, but, its specific molecular mechanisms in hepatoblastoma is not unknown. Methods: In this study, we estimated SNHG9 expression in hepatoblastoma tissue and cell lines by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). Next, we downregulated and upregulated SNHG9 expression in hepatoblastoma cell lines and then determined cell proliferation (CCK-8), colony formation, and cellular apoptosis activity. The dual luciferase reporter activity, RNA immunoprecipitation (RIP), biotin RNA pull down and Spemann's Pearson correlation coefficient assay were performed to establish the interaction between SNHG9, WNt3a and miR-23a-5p. A xenograft in-vivo tumorgenicity test was performed to elucidate the role of SNHG9 hepatoblastoma in tumorigenesis. SNHG9 role in Cisplatin drug resistance in hepatoblastoma was also determined. Results: SNHG9 was significantly upregulated in hepatoblastoma tissue and cell lines. SNHG9 overexpression on HUH6 & HepG2 resulted in a significant increase in cell proliferation and clonogenic activity while SNHG9 knock down resulted in a sustained inhibition of cell proliferation and clonogenic activity. Dual luciferase activity, RNA immunoprecipitation and biotin pull down confirmed the direct interaction of miR-23a-5p with SNHG9. The xenograft tumorgenicity test showed SNHG9 downregulation significantly inhibited the tumor growth in BALB/c mice. ROC and Kaplan-Meier analysis showed potential prognostic and diagnostic importance of SNHG9 in hepatoblastoma. Conclusion:We concluded that SNHG9/miR-23a-5p/Wnt3a axis promotes the progression hepatoblastoma tumor.

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Section: Discussionmentioning

confidence: 99%

SNHG9 promotes Hepatoblastoma Tumorigenesis via miR-23a-5p/Wnt3a Axis

Feng¹,

Bhandari²,

Liu³

et al. 2021

J. Cancer

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show abstract

“…The canonical Wnt signaling pathway participate in normal functioning of diverse physiological processes however, it`s abnormal aberrant activation resulting in development and progression of cancer (1,13,43,44). We identi ed miR23a-5p binding sites on Wnt3a using RNA hybrid database and showed reduced luciferase activity on HB cell lines co-transfected with Wnt3aWT and miR-23a-mimics.…”

Section: Discussionmentioning

confidence: 99%

SNHG9 Promotes the Hepatoblastoma Tumorigenesis via miR-23a-5p/Wnt3a Axis

Bhandari

Feng

Liu

et al. 2021

Preprint

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Background: Hepatoblastoma is common hepatic tumors occurring children between 0 – 5 years. Accumulating studies has shown lncRNA potential role in distinct cancers progression and development including the hepatoblastoma. SnoRNA host gene 9 (SNHG9) is associated the progression of distinct human cancers but, it`s specific molecular mechanisms in hepatoblastoma not unknown. Methods:In this study, we estimated SNHG9 expression on hepatoblastoma tissue and cell lines by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). Next, we downregulated and upregulated the SNHG9 expression in hepatoblastoma cell lines and then determined the cell proliferation (CCK-8), colony formation, cellular apoptosis activity. The dual luciferase reporter activity, RNA immunoprecipitation (RIP), biotin RNA pulls down and Spemann’s Pearson correlation coefficient assay were performed to establish the interaction between the SNHG9, WNt3a and miR-23a-5p. Xenograft in-vivo tumorgenicity test was performed to elucidate therole of SNHG9 hepatoblastoma in tumorigenesis. SNHG9 role in Cisplatin drugs resistance in hepatoblastoma was also determined. Results:SNHG9 was significantly upregulated in hepatoblastoma tissue and cell lines. SNHG9 overexpression on HUH6 & HepG2 resulted in a significant increase in cell proliferation and clonogeneic while SNHG9 knock down resulted in a sustained inhibition of cell proliferation and clonogenic activity. Dual luciferase activity, RNA immunoprecipitation and biotin pull down confirmed the direct interaction of miR-23a-5p with SNHG9. In Xenograft tumorgenicity test showed SNHG9 downregulation significantly reduced the tumor growth on mice. ROC and Kaplan-Meier analysis showed potential prognostic and diagnostic importance of SNHG9 in hepatoblastoma.Conclusion: We concluded that SNHG9/miR-23a-5p/Wnt3a axis promotes the progression hepatoblastoma tumor.

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“…Wnt/β-catenin canonical signaling has a vital function melanoma apoptosis, invasion, migration, proliferation, and differentiation. [20][21][22][23] The core component of the Wnt/β-catenin pathway, β-catenin, has an important function in tumor progression. 24 c-Myc can induce tumor cells to transition from the G1 phase to the S phase, thereby promoting cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

ENO1 Inhibits Apoptosis and Promotes Cell Invasion and Proliferation in Malignant Melanoma

Zhang

Tian

Zhang

et al. 2021

Preprint

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Introduction The glycolytic enzyme, α-Enolase (ENO1), catalyzes the production of phosphoenolpyruvate from 2-phosphoglycerate, which enhances glycolysis, and thus contributes to tumor progression. In the present study, we aimed to determine ENO1’s role in malignant melanoma (MM) and the potential underlying mechanism. Methods Western blotting was used to assess the levels of ENO1, c-Myc, β-catenin, MMP-9, PGAM1, and MMP-13 in MM-derived cell lines or tumor tissues from patients with MM. Plasmids pCMV-SPORT6-ENO1 and pET-28a-ENO1siRNA plasmids were used to overexpress and knockdown ENO1 in MM cells, respectively. To determine the function of ENO1 in the malignant behavior of MM cells, we performed wound healing, Cell counting kit 8, Transwell chamber, and flow cytometry analyses. Pyruvate determination and lactic acid kits were used to evaluate the production of pyruvate and lactic acid in tumor cells. Results The protein levels of ENO1 and PGAM1 in MM tissue were significantly higher than that in mole tissue. In MM cells, ENO1 overexpression inhibited apoptosis; promoted invasion, migration, and proliferation; increased pyruvate and lactate production; and increased in β-catenin, MMP-9, MMP-13, and c-Myc levels. The opposite effects were observed in MM cells silenced for ENO1. Conclusion These results indicated that ENO1 is involved in MM progression by enhancing invasion and proliferation, while inhibiting apoptosis. In addition, ENO1 might have an important function in tumor cell glycolysis. Therefore, ENO1 represents a potential therapeutic target to treat MM.

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Transcriptional Regulation of Wnt/β-Catenin Pathway in Colorectal Cancer

Cited by 165 publications

References 258 publications

SNHG9 promotes Hepatoblastoma Tumorigenesis via miR-23a-5p/Wnt3a Axis

SNHG9 promotes Hepatoblastoma Tumorigenesis via miR-23a-5p/Wnt3a Axis

SNHG9 Promotes the Hepatoblastoma Tumorigenesis via miR-23a-5p/Wnt3a Axis

ENO1 Inhibits Apoptosis and Promotes Cell Invasion and Proliferation in Malignant Melanoma

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Transcriptional Regulation of Wnt/β-Catenin Pathway in Colorectal Cancer

Cited by 165 publications

References 258 publications

SNHG9 promotes Hepatoblastoma Tumorigenesis via miR-23a-5p/Wnt3a Axis

SNHG9 promotes Hepatoblastoma Tumorigenesis via miR-23a-5p/Wnt3a Axis

SNHG9&nbsp;Promotes the Hepatoblastoma Tumorigenesis via miR-23a-5p/Wnt3a&nbsp;Axis

ENO1 Inhibits Apoptosis and Promotes Cell Invasion and Proliferation in Malignant Melanoma

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SNHG9 Promotes the Hepatoblastoma Tumorigenesis via miR-23a-5p/Wnt3a Axis