Biological functions and molecular interactions of Wnt/β-catenin in breast cancer: Revisiting signaling networks

Hashemi, Mehrdad; Hasani, Sahar; Hajimazdarany, Shima; Ghadyani, Fatemeh; Olyaee, Yeganeh; Khodadadi, Marzieh; Ziyarani, Maryam Fallah; Dehghanpour, Amir; Salehi, Hasti; Kakavand, Amirabbas; Goharrizi, Mohammad Ali Shekhi Beig; Aref, Amir Reza; Salimimoghadam, Shokooh; Akbari, Mohammad Esmaeil; Taheriazam, Afshin; Hushmandi, Kiavash; Entezari, Maliheh

doi:10.1016/j.ijbiomac.2023.123377

Cited by 14 publications

(8 citation statements)

References 224 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As we have shown, inhibition of WNT signalling does not prevent the ability to dedifferentiate, which again shows that dedifferentiation is due to amplifications of stemness genes, which also leads to their ectopic expression [39]. According to the literature, WNT signalling regulates several cellular functions that may explain the recovery from postchemotherapy shock: control and regulation of proliferation, repair of DNA damage, apoptosis inhibition and maintenance and regulation of embryonic properties and somatic and tumour stem cells [40,41]. Ectopic activation of WNT signalling, through activators amplifications and non-negative WNT regulator gene deletions, may be thought to activate tumour cell regeneration processes, by which they emerge from postchemotherapy shock, even in the absence of external signals, as in our cell cultures.…”

Section: Discussionmentioning

confidence: 75%

WNT-Conditioned Mechanism of Exit from Postchemotherapy Shock of Differentiated Tumour Cells

Tsydenova

Dolgasheva

Гаптулбарова

et al. 2023

Cancers

View full text Add to dashboard Cite

Background: the present study aims to prove or disprove the hypothesis that the state of copy number aberration (CNA) activation of WNT signalling pathway genes accounts for the ability of differentiated tumour cells to emerge from postchemotherapy shock. Methods: In the first step, the CNA genetic landscape of breast cancer cell lines BT-474, BT-549, MDA-MB-231, MDA-MD-468, MCF7, SK-BR-3 and T47D, which were obtained from ATCC, was examined to rank cell cultures according to the degree of ectopic activation of the WNT signalling pathway. Then two lines of T47D with ectopic activation and BT-474 without activation were selected. The differentiated EpCAM+CD44-CD24-/+ cells of these lines were subjected to IL6 de-differentiation with formation of mammospheres on the background of cisplatin and WNT signalling inhibitor ICG-001. Results: it was found that T47D cells with ectopic WNT signalling activation after cisplatin exposure were dedifferentiated to form mammospheres while BT-474 cells without ectopic WNT-signalling activation did not form mammospheres. The dedifferentiation of T47D cells after cisplatin exposure was completely suppressed by the WNT signalling inhibitor ICG-001. Separately, ICG-001 reduced, but did not abolish, the ability to dedifferentiate in both cell lines. Conclusions: these data support the hypothesis that the emergence of differentiated tumour cells from postchemotherapy shock after chemotherapy is due to ectopic activation of WNT signalling pathway genes.

show abstract

Section: Discussionmentioning

confidence: 75%

WNT-Conditioned Mechanism of Exit from Postchemotherapy Shock of Differentiated Tumour Cells

Tsydenova

Dolgasheva

Гаптулбарова

et al. 2023

Cancers

View full text Add to dashboard Cite

show abstract

“…β-catenin destruction complex and β-catenin degradation regulated by the ubiquitin-proteasome pathway are the core mechanisms regulating intracellular βcatenin levels [40] . The upregulation of Wnt is also commonly observed during progression of breast tumor and con rms that tumor cells are dependent on this pathway Wnt/β-catenin induction prevents apoptosis that is of importance for mediating drug resistance [41] . One study found that curcumin induced cytoskeletal remodeling through inhibition of Wnt/β-catenin signaling pathway, and the addition of curcumin also inhibited the EMT process [42] .…”

Section: Discussionmentioning

confidence: 92%

Traction force with extracellular matrix mediated by cytoskeleton had an effect on metastasis through SLC8A1 induced Wnt-β-catenin pathway in endometrial cancer

Zhou

et al. 2023

Preprint

View full text Add to dashboard Cite

Endometrial cancer (EC) is a common malignant tumor of female reproductive system. It seriously affects women's health. The mechanical characteristics of EC have not been paid noticed. However, the mechanical characteristics of different types of EC are diverse. These characteristics will greatly influence the development and prognosis of cancer cells. In this study, we explored traction force in primary EC cells and EC cell lines for the first time. It was found that the traction force of primary EC cells or cell lines with metastatic capability was lower. Various clinicopathological features of EC patients are significantly associated with traction force. In addition, we also confirmed that SLC8A1 is the main molecule which had an effect on traction force. The stiffness of extracellular matrix (ECM) had an influence on its downstream cytoskeleton expression through SLC8A1, thus changing the traction force and metastatic capacity of EC cells. The mechanism behind the SLC8A1 may be related to Wnt-β- catenin pathway and ion-channel activity. SLC8A1 can significantly regulate the downstream cytoskeleton F-actin and promote EC cell metastasis. Therefore, in this study, we found that SLC8A1 is an important molecule that affects the mechanical characteristics of endometrial cancer. The molecular mechanism is through changing the cytoskeleton by regulating Wnt- β- catenin pathway.

show abstract

“…Fuertes et al [ 42 ] found that non-classical WNT signaling promote colon tumor growth, chemotherapy resistance and tumor fibroblast activation. The up-regulation of WNT was observed in the progression of breast tumors and was associated with tumor drug resistance [ 43 ]. Wang et al [ 44 ] found that activating WNT signaling can promote cell growth and invasion of ccRCC.…”

Section: Discussionmentioning

confidence: 99%

Highly expressed of BID indicates poor prognosis and mediates different tumor microenvironment characteristics in clear cell renal cell carcinoma

Zeng,

Ke,

Tian

et al. 2024

Discov Onc

View full text Add to dashboard Cite

Background Studies have found that BH3 interacting domain death agonist (BID) is closely related to the occurrence and development of many kinds of tumors. However, little attention has been paid to the situation of BID in clear cell renal cell carcinoma (ccRCC). So, our aim was to explore the effect of BID in ccRCC. Methods Survival analysis, ROC curve, correlation analysis and Cox regression analysis were executed to analyze the prognostic value and clinical correlation of BID in ccRCC. The risk prognosis model was constructed in the training cohort and further validated in the internal testing cohort, ICGC cohort, and GEO cohort. Transcriptome sequencing and immunohistochemical staining of clinical specimens were used to validate the results of bioinformatics analysis. The GSEA, ESTIMATE algorithm, CIBERSORT algorithm, ssGSEA, TIDE score, correlation and difference analysis were used to analyze the effects of BID on immune infiltration in tumor microenvironment (TME). Results BID was highly expressed in ccRCC tissues, which was verified by transcriptome sequencing and immunohistochemical staining of clinical specimens. Patients with high expression of BID had a worse prognosis. BID is an independent prognostic factor for ccRCC. The prognostic model based on BID can accurately predict the prognosis of patients in different cohorts. In addition, the expression levels of BID was closely related to immunomodulatory molecules such as PD-1, LAG3, and CTLA4. Enrichment analysis indicated that BID was significantly enriched in immune-related responses and cancer-related pathways. The change of BID expression mediates different characteristics of immune infiltration in TME. Conclusions BID is highly expressed in ccRCC, which is a reliable biomarker of ccRCC prognosis. It is closely related to TME, and may be a potential target for immunotherapy in patients with ccRCC.

show abstract

Biological functions and molecular interactions of Wnt/β-catenin in breast cancer: Revisiting signaling networks

Cited by 14 publications

References 224 publications

WNT-Conditioned Mechanism of Exit from Postchemotherapy Shock of Differentiated Tumour Cells

WNT-Conditioned Mechanism of Exit from Postchemotherapy Shock of Differentiated Tumour Cells

Traction force with extracellular matrix mediated by cytoskeleton had an effect on metastasis through SLC8A1 induced Wnt-β-catenin pathway in endometrial cancer

Highly expressed of BID indicates poor prognosis and mediates different tumor microenvironment characteristics in clear cell renal cell carcinoma

Contact Info

Product

Resources

About