Naturally occurring compounds acting as potent anti‐metastatic agents and their suppressing effects on Hedgehog and <scp>WNT</scp>/β‐catenin signalling pathways

Farahmand, Leila; Darvishi, Behrad; Majidzadeh‐A, Keivan; Ansari, Alireza Madjid

doi:10.1111/cpr.12299

Cited by 24 publications

(12 citation statements)

References 113 publications

(190 reference statements)

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“…Wnt/β‐catenin signaling pathway has been reported to play a crucial role in multiple aspects of tumor progression, including NSCLC (Han et al, ; Seto et al, ; Tang et al, ). In addition, it has been known that Wnt/β‐catenin signaling pathway is involved in cancer invasion and metastasis (Farahmand, Darvishi, Majidzadeh‐A, & Ansari, ; Rong, Zhao, & Lu, ). For example, overexpressing lncRNA FOXD2‐AS1 can promote NSCLC progression through activating Wnt/β‐catenin signaling (Rong et al, ).…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA LINC00968 acts as oncogene in NSCLC by activating the Wnt signaling pathway

Wang

Zhou

Xu³

et al. 2017

Journal Cellular Physiology

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Long non-coding RNAs (lncRNAs) have played critical roles in a variety of cancers, including non-small cell lung cancer (N SCLC). In our study, we focused on the biological function and clinical significance of lncRNA LINC00968 in NSCLC. It was indicated that LINC00968 was significantly increased in LUAD tissues, LUSC tissues and NSCLC cells compared to their corresponding controls. Inhibition of LINC00968 was able to repress NSCLC growth, migration, and invasion in vitro while upregulation of LINC00968 reversed this process. Additionally, downregulation of LINC00968 induced apoptosis capacity of A549 cell. Apoptosis-related proteins BCL-2 were decreased and BAX was increased by knockdown of LINC00968, respectively. Meanwhile we observed that Wnt signaling pathway was involved in the LINC00968-induced NSCLC progression. Finally, in vivo tumor xenografts were established using A549 cells to detect the function of LINC00968 in NSCLC tumorigenesis. Silencing LINC00968 greatly inhibited NSCLC tumor progression, which was consistent with the in vitro tests. In conclusion, we have uncovered that LINC00968 could be regarded as a novel prognostic biomarker and therapeutic target in NSCLC diagnosis and treatment.

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Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA LINC00968 acts as oncogene in NSCLC by activating the Wnt signaling pathway

Wang

Zhou

Xu³

et al. 2017

Journal Cellular Physiology

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“…In our previous study, we revealed that WNT signalling genes were downregulated in the IC rat model 13 . The WNT signalling pathway is known to modulate tissue fibrosis and associated EMT processes 21 . Thus, we further investigated the association of fibrosis with WNT signalling cascades in IC/BPS patients.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of WNT11 is associated with bladder tissue fibrosis in patients with interstitial cystitis/bladder pain syndrome without Hunner lesion

Choi

Han

Shin

et al. 2018

Sci Rep

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This study assessed the functional role of WNT genes and the association between WNT signalling cascades and fibrosis in interstitial cystitis/bladder pain syndrome (IC/BPS) patients. Twenty-five patients (3 males, 22 females; mean age 59.7 ± 10.9 years), included 7 non-Hunner-type IC (NHIC), 18 Hunner-type IC (HIC), and 5 non-IC (control) groups. The expression of sonic hedgehog, WNT gene family, and genes previously reported as biomarkers for IC/BPS were examined using RT-PCR in biopsy specimens from the mucosa and submucosa layer of the bladder. WNT2B, WNT5A, WNT10A, and WNT11 functions in the urothelium were evaluated by silencing in an HBlEpC cell line. Pelvic Pain and Urgency/Frequency Patient Symptom Scale scores, O’Leary-Sant Symptom and Problem Index scores, and Visual Analogue Scores did not differ between the NHIC and HIC groups. However, HIC patients had significantly shorter symptom duration (30.9 vs 70.8 months, p = 0.046), higher daily urinary frequency (16.1 versus 8.5 times, p = 0.006), and smaller bladder capacity (208.6 versus 361.4 ml, p = 0.006) than NHIC patients. Overall WNT gene expression was lower in NHIC than HIC patients. Bladder epithelial tissues from HIC patients were characterised by the downregulation of WNT11. Silencing of WNT11, WNT2B, WNT5A, and WNT10A in HBlEpCs resulted in fibrotic changes, indicated by fibrotic morphology, increased fibrosis-related gene expression, and nuclear localisation of phosphorylated SMAD2, and increased vimentin and fibronectin levels. Downregulation of WNT11 results in fibrotic changes of bladder epithelial cells and is associated with the pathogenesis and differential diagnosis of NHIC. Decreased expression of WNT11 is a potential biomarker for predicting NHIC.

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“…1 ). According to current researches, deregulation of the Wnt signaling pathway is related to tumor propagation, invasion, and development of resistance to anticancer agents which steer tumors toward a malignant form of progression, and ultimately leading to poor prognosis of overall survival [ 6 , 7 ]. Interestingly, recent findings in TNBC tumors have elucidated the crosstalk between the Wnt pathway and multiple growth factors and developmental signaling pathways and β-catenin as a main downstream effector of the pathway at multiple levels [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Triple-negative breast cancer: understanding Wnt signaling in drug resistance

2021

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Triple-negative breast cancer (TNBC) is not as prevalent as hormone receptor or HER2-positive breast cancers and all receptor tests come back negative. More importantly, the heterogeneity and complexity of the TNBC on the molecular and clinical levels have limited the successful development of novel therapeutic strategies and led to intrinsic or developed resistance to chemotherapies and new therapeutic agents. Studies have demonstrated deregulation of Wnt/β-catenin signaling in tumorigenesis which plays decisive roles at the low survival rate of patients and facilitates resistance to currently existing therapies. This review summarizes mechanisms of Wnt/β-catenin signaling for resistance development in TNBC, the complex interaction between Wnt/β-catenin signaling, and the transactivated receptor tyrosine kinase (RTK) signaling pathways, lymphocytic infiltration, epithelial-mesenchymal transition (EMT), and induction of metastasis. Such associations and how these pathways interact in the development and progression of cancer have led to the careful analysis and development of new and effective combination therapies without generating significant toxicity and resistance.

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Naturally occurring compounds acting as potent anti‐metastatic agents and their suppressing effects on Hedgehog and WNT/β‐catenin signalling pathways

Cited by 24 publications

References 113 publications

Long non‐coding RNA LINC00968 acts as oncogene in NSCLC by activating the Wnt signaling pathway

Long non‐coding RNA LINC00968 acts as oncogene in NSCLC by activating the Wnt signaling pathway

Downregulation of WNT11 is associated with bladder tissue fibrosis in patients with interstitial cystitis/bladder pain syndrome without Hunner lesion

Triple-negative breast cancer: understanding Wnt signaling in drug resistance

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