Periostin in tumor microenvironment is associated with poor prognosis and platinum resistance in epithelial ovarian carcinoma

Sung, Pi Lin; Jan, Yi-Hua; Lin, Shih Chieh; Huang, Chao; Lin, Hao; Wen, Kuo Chang; Chao, Kuan Chong; Lai, Chiung Ru; Wang, Peng Hui; Chuang, Chi Mu; Wu, Hua Hsi; Twu, Nae Fang; Yen, Ming Shyen; Hsiao, Michael; Huang, Chi Ying F.

doi:10.18632/oncotarget.6700

Cited by 70 publications

(91 citation statements)

References 39 publications

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“…However, over 80 ~ 90% patients are diagnosed at the advanced stage, which attributed to the early metastasis and dissemination of the PaC cells [3]. POSTN, originally designated osteoblast-specific factor 2, was found to be overexpressed in various types of human tumors [30, 31], including PaC [1, 32]. POSTN mRNA elevated 42-fold in PaC, and patients with increased expression had a shorter survival tendence [1].…”

Section: Discussionmentioning

confidence: 99%

Periostin promotes tumor angiogenesis in pancreatic cancer via Erk/VEGF signaling

Liu

Gao

et al. 2016

Oncotarget

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Pancreatic cancer (PaC) consists of a bulk of stroma cells which contribute to tumor progression by releasing angiogenic factors. Recent studies have found that periostin (POSTN) is closely associate with the metastatic potential and prognosis of PaC. The purpose of this study is to determine the role of POSTN in tumor angiogenesis and explore the precise mechanisms. In this study, we used lentiviral shRNA and human recombinant POSTN protein (rPOSTN) to negatively and positively regulate POSTN expression in vitro. We found that increased POSTN expression promoted the tubule formation dependent on human umbilical vein endothelial cells (HUVECs). Moreover, knockdown of POSTN in PaC cells reduced tumor growth and VEGF expression in vivo. In accordance with these observations, we found that Erk phosphorylation and its downstream VEGF expression were upregulated achieved in rPOSTN-treated groups, opposing results were obversed in POSTN-slienced group. Meanwhile, Erk inhibitor SCH772984 significantly decreased VEGF expression as well as tubule formation of HUVECs in rPOSTN-treated PaC cells. Taken together, these findings suggest that POSTN promotes tumor angiogenesis via Erk/VEGF signaling in PaC and POSTN may be a new target for cancer anti-vascular treatment.

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Section: Discussionmentioning

confidence: 99%

Periostin promotes tumor angiogenesis in pancreatic cancer via Erk/VEGF signaling

Liu

Gao

et al. 2016

Oncotarget

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“…Treatment with recombinant periostin promoted ES-2 cell resistance to both carboplatin and paclitaxel in vitro (Ryner et al 2015). A recent study has shown stromal periostin and not tumour periostin is an independent predictor of OS and DFS in epithelial ovarian cancer (Sung et al 2016). Using the CSIOVDB , POSTN expression was significantly increased in tumour stroma and peritoneal tumours compared with that in primary ovarian tumours.…”

Section: Role Of Periostin In Ovarian Cancermentioning

confidence: 99%

WOMEN IN CANCER THEMATIC REVIEW: Ovarian cancer–peritoneal cell interactions promote extracellular matrix processing

Ricciardelli

Lokman

Ween

et al. 2016

Endocrine-Related Cancer

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Ovarian cancer has a distinct tendency for metastasising via shedding of cancerous cells into the peritoneal cavity and implanting onto the peritoneum that lines the pelvic organs. Once ovarian cancer cells adhere to the peritoneal cells, they migrate through the peritoneal layer and invade the local organs. Alterations in the extracellular environment are critical for tumour initiation, progression and intra-peritoneal dissemination. To increase our understanding of the molecular mechanisms involved in ovarian cancer metastasis and to identify novel therapeutic targets, we recently studied the interaction of ovarian cancer and peritoneal cells using a proteomic approach. We identified several extracellular matrix (ECM) proteins including, fibronectin, TGFBI, periostin, annexin A2 and PAI-1 that were processed as a result of the ovarian cancerperitoneal cell interaction. This review focuses on the functional role of these proteins in ovarian cancer metastasis. Our findings together with published literature support the notion that ECM processing via the plasminogen-plasmin pathway promotes the colonisation and attachment of ovarian cancer cells to the peritoneum and actively contributes to the early steps of ovarian cancer metastasis.

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“…For inhibitor treatment in 2D and 3D cultures, 100 nM of rapamycin (Grabiner et al, 2014;Kang et al, 2013;Sarbassov et al, 2006), 250 nM of Torin1 (Cheng et al, 2016;Grabiner et al, 2014;Kang et al, 2013;Thoreen et al, 2012), 10 μM of PF47068671 (Pearce et al, 2010;Schipany et al, 2015;Zhang et al, 2015), 1 μM of MK2206 (Devery et al, 2015;Shen et al, 2015;Sung et al, 2016) and 1 μM of AZD6244 (Devery et al, 2015;Ewald et al, 2015) were employed as these concentrations have been most frequently used in cell-based assays and have a complete effect on their respective targets [ phospho-protein analysis in western blots (see Fig. 4 and western blots in the supporting figures)].…”

Section: Inhibitor Treatmentmentioning

confidence: 99%

Comparison of cancer cells cultured in 2D vs 3D reveals differences in AKT/mTOR/S6-kinase signaling and drug response

Riedl

Schlederer

Pudelko

et al. 2016

Journal of Cell Science

358

293

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Three-dimensional (3D) cancer models are used as preclinical systems to mimic physiologic drug responses. We provide evidence for strong changes of proliferation and metabolic capacity in three dimensions by systematically analyzing spheroids of colon cancer cell lines. Spheroids showed relative lower activities in the AKT, mammalian target of rapamycin (mTOR) and S6K (also known as RPS6KB1) signaling pathway compared to cells cultured in two dimensions. We identified spatial alterations in signaling, as the level of phosphorylated RPS6 decreased from the spheroid surface towards the center, which closely coordinated with the tumor areas around vessels in vivo. These 3D models displayed augmented antitumor responses to AKT-mTOR-S6K or mitogen-activated protein kinase (MAPK) pathway inhibition compared to those in 2D models. Inhibition of AKT-mTOR-S6K resulted in elevated ERK phosphorylation in 2D culture, whereas under these conditions, ERK signaling was reduced in spheroids. Inhibition of MEK1 (also known as MAP2K1) led to decreased AKT-mTOR-S6K signaling in 3D but not in 2D culture. These data indicate a distinct rewiring of signaling in 3D culture and during treatment. Detached tumor-cell clusters in vessels, in addition to circulating single tumor cells, play a putative role in metastasis in human cancers. Hence, the understanding of signaling in spheroids and the responses in the 3D models upon drug treatment might be beneficial for anti-cancer therapies.

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Periostin in tumor microenvironment is associated with poor prognosis and platinum resistance in epithelial ovarian carcinoma

Cited by 70 publications

References 39 publications

Periostin promotes tumor angiogenesis in pancreatic cancer via Erk/VEGF signaling

Periostin promotes tumor angiogenesis in pancreatic cancer via Erk/VEGF signaling

WOMEN IN CANCER THEMATIC REVIEW: Ovarian cancer–peritoneal cell interactions promote extracellular matrix processing

Comparison of cancer cells cultured in 2D vs 3D reveals differences in AKT/mTOR/S6-kinase signaling and drug response

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