WNT-1 inducible signaling pathway protein-1 enhances growth and tumorigenesis in human breast cancer

Chiang, Kun‐Chun; Yeh, Chun‐Nan; Chung, Li-Chuan; Feng, Tsui-Hsia; Sun, Chi-Chin; Chen, Miin‐Fu; Jan, Yi-Yin; Yeh, Ta‐Sen; Chen, Shin‐Cheh; Juang, Horng‐Heng

doi:10.1038/srep08686

Cited by 65 publications

(82 citation statements)

References 43 publications

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“…Importantly, aberrant function or dysregulation of the Wisp1 signaling is associated with a variety of disorders, including musculoskeletal, vascular and neurodegenerative (Maiese 2014), as well as various cancers (Gurbuz & Chiquet-Ehrismann 2015), including breast (Chiang et al 2015), prostate (Ono et al 2013) and gastrointestinal (White et al 2012). In the present study, we identify Wisp1 as a novel mediator of Bmp3-induced MSC proliferation, a key but poorly understood component of adipogenesis.…”

Section: Discussionmentioning

confidence: 71%

Wisp1 mediates Bmp3-stimulated mesenchymal stem cell proliferation

Cernea¹,

Tang²,

Guan³

et al. 2015

Journal of Molecular Endocrinology

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Adipose tissue expansion, resulting from adipocyte hyperplasia and/or hypertrophy, is a hallmark of obesity. Adipocytes are derived from mesenchymal stem cells (MSCs) through adipogenesis, a process involving three key steps: proliferation, commitment and differentiation. Although studies have elaborated on the mechanisms regulating adipocyte commitment and differentiation, the factors that control MSC proliferation remain largely unknown. Previously, we demonstrated that bone morphogenetic protein 3 (Bmp3), the expression of which was upregulated in our rat model of hyperplasic visceral adiposity, potently stimulated MSC proliferation. In the present study, we investigate the molecular target of Bmp3. We conducted DNA microarray analysis on MSCs treated with and without Bmp3 and identified WNT1-inducible signaling pathway protein 1 (Wisp1) as a differentially expressed gene, whose expression was upregulated 3.7-fold by Bmp3. Wisp1 is a proliferative agent in various non-adipose cell types and is implicated in adipogenesis. Therefore, we tested the hypothesis that Wisp1 mediates Bmp3 stimulation of MSC proliferation. We showed that Bmp3 increased the expression of Wisp1 as early as 3 h following Bmp3 treatment in MSCs. Importantly, the upregulated Wisp1 expression preceded Bmp3-induced MSC proliferation, as determined by [ 3 H]-thymidine incorporation.Furthermore, treatment of MSCs with recombinant Wisp1 led to a concentration-dependent increase in [ 3 H]-thymidine incorporation with a maximal increase of 300%. In addition, siRNA-mediated knockdown of Wisp1 expression attenuated Bmp3-induced MSC proliferation. Taken together, our present findings reveal Wisp1 as a novel target of Bmp3 and suggest that the Bmp3/Wisp1 signaling pathway play a key role in MSC proliferation, and consequently adipogenesis.

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Section: Discussionmentioning

confidence: 71%

Wisp1 mediates Bmp3-stimulated mesenchymal stem cell proliferation

Cernea¹,

Tang²,

Guan³

et al. 2015

Journal of Molecular Endocrinology

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“…20 On the contrary, WISP-1 was also found to negatively regulate the progress of cell motility and invasion by the inhibition of Rac function through integrins in lung cancer. 16,20 Although WISP-1 has been increasingly investigated in different types of cancer, because of the complicated functions and mechanisms of WISP-1 on mediating the occurrence and progression in different types of cancer, the accurate biological effect of WISP-1 on GC was still completely unrevealed in current research.…”

Section: Discussionmentioning

confidence: 99%

“…This result was supported by the previous studies on endometrial endometrioid adenocarcinoma, breast cancer, and some other tumor types. 8,16 The associations of WISP-1 with cancer cell biological processes were also revealed in recent studies, but the exact biological role and the related molecular mechanism were disparate. Oral squamous cell carcinoma (OSCC) was one tumor type that clearly presented the molecular mechanisms which were mediated by WISP-1 in recent years.…”

Section: Discussionmentioning

confidence: 99%

“…Recent researches revealed that WISP-1 inhibited non-small cell lung cancer cell migration and invasion, whereas it accelerated the cell invasion and metastasis of colorectal carcinoma and breast cancer. 12,16,17 Therefore, to explore the role of WISP-1 in GC progression, we investigated the relationship of WISP-1 with migration and invasion, which were essential characteristics in mediating tumorigenesis. As expected, in scratch wounding assay, knockdown of WISP-1 significantly inhibited GC cell migration (Figure 3(a)), and this result was corresponding to the result which was demonstrated by the transwell chamber migration assay (Figure 3(b)).…”

Section: Loss Of Wisp-1 Reduced Gc Cell Proliferation Migration and mentioning

confidence: 99%

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Association of Wnt1-inducible signaling pathway protein-1 with the proliferation, migration and invasion in gastric cancer cells

Jia

Feng

et al. 2017

Tumour Biol.

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Wnt1-inducible signaling pathway protein-1 is a cysteine-rich protein that belongs to the CCN family, which has been implicated in mediating the occurrence and progression through distinct molecular mechanisms in several tumor types. However, the association of Wnt1-inducible signaling pathway protein-1 with gastric cancer and the related molecular mechanisms remain to be elucidated. Therefore, this study aimed to clarify the biological role of Wnt1-inducible signaling pathway protein-1 in the proliferation, migration, and invasion in gastric cancer cells and further investigated the associated molecular mechanism on these biological functions. We first detected the expression level of Wnt1-inducible signaling pathway protein-1 in gastric cancer, and the reverse transcription polymerase chain reaction have shown that Wnt1-inducible signaling pathway protein-1 expression levels were upregulated in gastric cancer tissues. The expression of Wnt1-inducible signaling pathway protein-1 in gastric cancer cell lines was also detected by quantitative real-time polymerase chain reaction and Western blotting. Furthermore, two gastric cancer cell lines with high expression of Wnt1-inducible signaling pathway protein-1 were selected to explore the biological function of Wnt1-inducible signaling pathway protein-1 in gastric cancer. Function assays indicated that knockdown of Wnt1-inducible signaling pathway protein-1 suppressed cell proliferation, migration, and invasion in BGC-823 and AGS gastric cancer cells. Further investigation of mechanisms suggested that cyclinD1 was identified as one of Wnt1-inducible signaling pathway protein-1 related genes to accelerate proliferation in gastric cancer cells. In addition, one pathway of Wnt1-inducible signaling pathway protein-1 induced migration and invasion was mainly through the enhancement of epithelial-to-mesenchymal transition progression. Taken together, our findings presented the first evidence that Wnt1-inducible signaling pathway protein-1 was upregulated in gastric cancer and acted as an oncogene by promoting proliferation, migration, and invasion in gastric cancer cells.

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“…Ectopic expression of WISP1 in breast cancer cells promotes cell growth and metastasis, represses p21 and p27 expression, and stimulates EMT. WISP1, NDRG1, a tumor suppressor gene for breast cancer, is repressed by WISP1 through DNA sequences within the NDRG1 promoter [45]. Thus, WISP1 is a human breast cancer oncogene and is a potential therapeutic target.…”

Section: Wispmentioning

confidence: 99%

Advancement of Wnt signal pathway and the target of breast cancer

Qin

Zhao

et al. 2016

Open Life Sciences

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Wnt/β-catenin signaling has been proved to play an important role in the development and promotion of cancer metastasis. The activation of Wnt signals can lead to duplicating, updating, metastasizing and relapsing. The Wnt signaling pathway is mainly divided into the Wnt/β-catenin pathway and the Wnt/calcium pathway. A better understanding of all the diverse functions of Wnt and their molecular mechanisms has evoked prevailing interest in identifying additional targets related to the Wnt /β-catenin pathways in breast cancer. A number of new target, related to Wnt /β-catenin pathways have been identified in recent years, including NOP14, BKCa channels, Emilin2, WISP, MicroRNAs, NRBP1, TRAF4, and Wntless. In this review, we will introduce the new targets related to the Wnt /β-catenin pathways in breast cancer.

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WNT-1 inducible signaling pathway protein-1 enhances growth and tumorigenesis in human breast cancer

Cited by 65 publications

References 43 publications

Wisp1 mediates Bmp3-stimulated mesenchymal stem cell proliferation

Wisp1 mediates Bmp3-stimulated mesenchymal stem cell proliferation

Association of Wnt1-inducible signaling pathway protein-1 with the proliferation, migration and invasion in gastric cancer cells

Advancement of Wnt signal pathway and the target of breast cancer

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