Antagonizing canonical Wnt signaling pathway by recombinant human sFRP4 purified from E. coli and its implications in cancer therapy

Ghoshal, Archita; Ghosh, Siddhartha Sankar

doi:10.1007/s11010-016-2738-6

Cited by 12 publications

(5 citation statements)

References 61 publications

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“…It can inhibit the activation of the Wnt signaling pathway by competitively binding with receptors related to the Wnt signaling pathway. The present data indicated that the expression levels of SFRP4 were decreased at both the mRNA and protein levels in FLS, which was in accordance with findings from other relevant research studies (77,78). Notably, after lncRNAS56464.1 interference, the expression of SFRP4 was significantly increased.…”

Section: Discussionsupporting

confidence: 92%

lncRNAS56464.1 as a ceRNA promotes the proliferation of fibroblast‑like synoviocytes in experimental arthritis via the Wnt signaling pathway and sponges miR‑152‑3p

et al. 2021

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Rheumatoid arthritis (RA) is an autoimmune disease that occurs in approximately 1.0% of the general population. In RA patients, physical disability and joint damage are the major prognostic factors, which are associated with a reduction in the quality of life and early mortality. At present, the exact molecular mechanism of RA remains elusive. Long noncoding RNAs (lncRNAs) have been revealed to play a regulatory role in the pathogenesis of RA. To reveal the function of lncRNAs in rheumatoid arthritis, lncRNAS56464.1 was screened to verify its targeting of the microRNA (miR)-152-3p/Wnt pathway and its effect on the proliferation of fibroblast-like synoviocytes (FLS). In the present study, based on the competing endogenous RNA (ceRNA) theory, siRNA was designed for transfection into FLS to calculate the lncRNAS56464.1 interference efficiency and then the effect of lncRNAS56464.1 interference on FLS proliferation was detected by MTT assay. Then, lncRNAS56464.1 targeting of the miR-152-3p/Wnt pathway was detected by a dual-luciferase reporter assay. In addition, RT-qPcR, immunofluorescence and western blotting techniques were employed to detect the expression of lncRNAS56464.1, miR-152-3p and some key genes of the Wnt signaling pathway in FLS after lncRNAS56464.1 interference. The results revealed that lncRNAS56464.1 could combine with miR-152-3p and promoted the proliferation of FLS. In addition, lncRNAS56464.1 interference could not only decrease the proliferation of FLS and the expression of Wnt1, β-catenin, c-Myc, cyclin d1, and p-GSK-3β/GSK-3β, but it also increased the expression of SFRP4. The present data indicated that lncRNAS56464.1 could target the miR-152-3p/Wnt pathway to induce synovial cell proliferation and then participate in the pathogenesis of RA.

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Section: Discussionsupporting

confidence: 92%

lncRNAS56464.1 as a ceRNA promotes the proliferation of fibroblast‑like synoviocytes in experimental arthritis via the Wnt signaling pathway and sponges miR‑152‑3p

et al. 2021

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“…Activation of the canonical WNT pathway has been described to affect proliferation and migration of various non-rhabdomyomatous tumor cells through induction of the targets such as the pro-proliferative protein MYC and the pro-proliferative and anti-apoptotic IAP-protein BIRC5 (survivin) (29, 30). We here tested the effects of FH535, XAV939, β-catenin siRNA, and WNT3A treatment on proliferation and expression of the mentioned β-catenin target genes in the above mentioned RMS cell lines.…”

Section: Resultsmentioning

confidence: 99%

Canonical WNT/β-Catenin Signaling Plays a Subordinate Role in Rhabdomyosarcomas

et al. 2018

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The development of skeletal muscle from immature precursors is partially driven by canonical WNT/β-catenin signaling. Rhabdomyosarcomas (RMS) are immature skeletal muscle-like, highly lethal cancers with a variably pronounced blockade of muscle differentiation. To investigate whether canonical β-catenin signaling in RMS is involved in differentiation and aggressiveness of RMS, we analyzed the effects of WNT3A and of a siRNA-mediated or pharmacologically induced β-catenin knock-down on proliferation, apoptosis and differentiation of embryonal and alveolar RMS cell lines. While the canonical WNT pathway was maintained in all cell lines as shown by WNT3A induced AXIN expression, more distal steps including transcriptional activation of its key target genes were consistently impaired. In addition, activation or inhibition of canonical WNT/β-catenin only moderately affected proliferation, apoptosis or myodifferentiation of the RMS tumor cells and a conditional knockout of β-catenin in RMS of Ptchdel/+ mice did not alter RMS incidence or multiplicity. Together our data indicates a subordinary role of the canonical WNT/β-catenin signaling for RMS proliferation, apoptosis or differentiation and thus aggressiveness of this malignant childhood tumor.

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“…Wnt/β-catenin signaling has been demonstrated to serve an important role in regulating tumor initiation and progression in various malignant tumor types, including lung cancer and HCC ( 27 , 28 ). Furthermore, Wnt signaling may regulate genes that are involved in cell-cycle regulation and cell apoptosis, including Cyclin and Bcl-2 ( 29 ).…”

Section: Discussionmentioning

confidence: 99%

Suppression of tumor cell proliferation and migration by human umbilical cord mesenchymal stem cells: A possible role for apoptosis and Wnt signaling

et al. 2018

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Human umbilical cord-derived mesenchymal stem cells (hUCMSCs) represent potential therapeutic tools for solid tumors. However, there are numerous inconsistent results regarding the effects of hUCMSCs on tumors, and the mechanisms underlying this remain poorly understood. The present study further examined this controversial issue by analyzing the molecular mechanisms of the inhibitory effects of hUCMSCs on the proliferation and migration of the human lung cancer A549 cell line and the human hepatocellular carcinoma (HCC) BEL7402 cell line in vitro. Flow cytometric analysis demonstrated that hUCMSCs arrested tumor cells in specific phases of the cell cycle and induced the apoptosis of tumor cells by using the hUCMSC-conditioned medium (hUCMSC-CM). The hUCMSC-CM also attenuated the migratory abilities of the two tumor cell types. Furthermore, the expression of B-cell lymphoma 2 (Bcl-2), the pro-form of caspase-7 (pro-caspase-7), β-catenin and c-Myc was downregulated, while that of ephrin receptor (EphA5), a biomarker of cancer cell dormancy, was slightly increased in these two tumor cell lines treated with hUCMSC-CM. Specifically, when co-cultured via direct cell-to-cell contact, hUCMSCs were able to spontaneously fuse with any of the two types of solid tumor cells. These observations suggested that hUCMSCs may be a promising candidate for the biological therapy of lung cancer and HCC. Future studies should focus on detailed evidence for cell fusion, as well as other mechanisms proposed in the present study, by introducing additional experimental approaches and models.

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Antagonizing canonical Wnt signaling pathway by recombinant human sFRP4 purified from E. coli and its implications in cancer therapy

Cited by 12 publications

References 61 publications

lncRNAS56464.1 as a ceRNA promotes the proliferation of fibroblast‑like synoviocytes in experimental arthritis via the Wnt signaling pathway and sponges miR‑152‑3p

lncRNAS56464.1 as a ceRNA promotes the proliferation of fibroblast‑like synoviocytes in experimental arthritis via the Wnt signaling pathway and sponges miR‑152‑3p

Canonical WNT/β-Catenin Signaling Plays a Subordinate Role in Rhabdomyosarcomas

Suppression of tumor cell proliferation and migration by human umbilical cord mesenchymal stem cells: A possible role for apoptosis and Wnt signaling

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