Impact by pancreatic stellate cells on epithelial-mesenchymal transition and pancreatic cancer cell invasion: Adding a third dimension in vitro

Karnevi, Emelie; Rosendahl, Ann H.; Hilmersson, Katarzyna Said; Saleem, Moin A.; Andersson, Roland

doi:10.1016/j.yexcr.2016.07.017

Cited by 35 publications

(40 citation statements)

References 43 publications

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“…Cells do not migrate in a monoculture setup or when macrophages are cultured underneath transwells 60. c) BxPC‐3 pancreatic cancer cells migrate into a Matrigel/collagen I hydrogel blend when cultured with M2 macrophages 60,65…”

Section: Coculture Effects On Cell Movement Through Hydrogelsmentioning

confidence: 99%

“…Although it is becoming increasingly accepted that macrophage polarization states exist on a spectrum and are unique to the microenvironment,64,65 M1 and M2 polarized macrophages are used to model proinflammatory and tissue remodeling, respectively. Some studies have polarized macrophages to an M2 state using interleukin‐4 (IL‐4) and IL‐13 to model advanced stage tumors where CD163+ cells make up the majority of this cell population 65. Karnevi et al studied the influence of M2 macrophages on BxPC‐3 pancreatic cancer cell invasion into a blend of Matrigel and collagen I 65.…”

Section: Coculture Effects On Cell Movement Through Hydrogelsmentioning

confidence: 99%

See 1 more Smart Citation

Designer Biomaterials to Model Cancer Cell Invasion In Vitro: Predictive Tools or Just Pretty Pictures?

Bahlmann

Smith

Shoichet

2020

Adv Funct Materials

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Metastasis is the leading cause of mortality in cancer patients. Underlying this process is the invasion and colonization of cancer cells into healthy tissues. Engineered hydrogel models of tumor microenvironments present an opportunity to understand the microenvironmental determinants of cellular invasion. The biochemical and mechanical cues, presented in the form of adhesion sites, degradable cues, matrix stiffness, and architecture, have significant effects on the extent of cancer cell migration, and the mechanisms employed by these cells to move through their matrix. Coculture with stromal cells such as cancer associated fibroblasts, endothelial cells, and immune cells that are associated with poor prognosis demonstrate that these cells exacerbate cancer cell invasion. With these models, researchers aim not only to recapitulate known cancer cell behaviors in a dish, but also to uncover new insights into mechanisms underlying these phenomena, paving the way for novel treatment strategies. In this perspective, the design of engineered models that are used to study cancer cell invasion and metastasis in vitro is discussed. To this end, the authors seek to understand and put into perspective: do these models reveal relevant mechanisms of cancer cell migration, or are they simply pretty pictures with little biological translatability?

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Section: Coculture Effects On Cell Movement Through Hydrogelsmentioning

confidence: 99%

Section: Coculture Effects On Cell Movement Through Hydrogelsmentioning

confidence: 99%

Designer Biomaterials to Model Cancer Cell Invasion In Vitro: Predictive Tools or Just Pretty Pictures?

Bahlmann

Smith

Shoichet

2020

Adv Funct Materials

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“…Pancreatic cancer cells can induce MDSCs that promote tumor cell survival and accumulation [143]–EMTAngiogenesisImmunosuppressionPSCs1. PSCs decrease the expression of E-carderin and ZO-1, increase the expression of β-catenin and vimentin in pancreatic cancer cells [116, 144]2. IL-6 from PSCs promote EMT in PDAC cells via Stat3/Nrf2 pathway [145]1.…”

Section: Interactions and Mechanisms Between Stromal Cells And Pancrementioning

confidence: 99%

Chemotherapy and tumor microenvironment of pancreatic cancer

2017

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Pancreatic cancer is an extremely dismal malignance. Chemotherapy has been widely applied to treat this intractable tumor. It has exclusive tumor microenvironment (TME), characterized by dense desmoplasia and profound infiltrations of immunosuppressive cells. Interactions between stromal cells and cancer cells play vital roles to affect the biological behaviors of pancreatic cancer. Targeting the stromal components of pancreatic cancer has shown promising results. In addition to the direct toxic effects of chemotherapeutic drugs on cancer cells, they can also remodel the TME, eventually affecting their efficacy. Herein, we reviewed the following four aspects; (1) clinical landmark advances of chemotherapy in pancreatic cancer, since 2000; (2) interactions and mechanisms between stromal cells and pancreatic cancer cells; (3) remodeling effects and mechanisms of chemotherapy on TME; (4) targeting stromal components in pancreatic cancer.Electronic supplementary materialThe online version of this article (doi:10.1186/s12935-017-0437-3) contains supplementary material, which is available to authorized users.

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“…Epithelial-mesenchymal transition (EMT) of tumor cells induced by stromal cells has been reported (62)(63)(64). EMT is a key event in tumor invasion and metastasis, whereby epithelial cell layers lose polarity and cell-cell contacts, and undergo marked cytoskeletal remodeling (65).…”

Section: Effect Of Preoperative Therapy On Pancreatic Cancer Tissuesmentioning

confidence: 99%

Neoadjuvant chemotherapy for pancreatic cancer: Effects on cancer tissue and novel perspectives

et al. 2017

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Abstract. Chemotherapy for pancreatic cancer has diversified following the addition of more treatment regimens; however, in spite of this, pancreatic cancer remains a fatal disease. Preoperative (neoadjuvant) chemotherapy (NAC) or neoadjuvant chemoradiation therapy (NACRT) has been developed and implemented. For patients with borderline resectable pancreatic cancer (BRPC) and locally advanced pancreatic cancer (LAPC), a number of clinical trials have been conducted; NACRT was demonstrated to improve resectability, R0 resection rate, overall survival rate, disease-free survival rate and even an LAPC and BRPC survival advantage over NAC. However, from the knowledge obtained from resected specimens following preoperative treatment, residual pancreatic cancer tissues following NAC are rich in chemoresistant cancer stem-like cells and epithelial-mesenchymal transition (EMT) markers. Conversely, metformin, angiotensin receptor blocker, statins and low-dose paclitaxel are well-known as drugs that inhibit EMT, which is associated with cancer stem cell-like characteristics. Although clinical effectiveness is unlikely to be achieved using one of these as an anticancer agent, it is reasonable to use these drugs for patients with comorbidities in the treatment of pancreatic cancer. Furthermore, gemcitabine (GEM) affects antitumor immunity by stimulating the expression of major histocompatibility complex class I-related chain A on the surface of cancer cells to enhance the cytotoxicity of natural killer cells. Considering EMT and antitumor immunity, there is a possibility that GEM and nanoparticle albumin-bound paclitaxel therapy is the most suitable regimen for treating pancreatic cancer. However, even as preoperative treatment progresses, R0 resection is the most important factor for the long-term survival of pancreatic cancer patients.

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Impact by pancreatic stellate cells on epithelial-mesenchymal transition and pancreatic cancer cell invasion: Adding a third dimension in vitro

Cited by 35 publications

References 43 publications

Designer Biomaterials to Model Cancer Cell Invasion In Vitro: Predictive Tools or Just Pretty Pictures?

Designer Biomaterials to Model Cancer Cell Invasion In Vitro: Predictive Tools or Just Pretty Pictures?

Chemotherapy and tumor microenvironment of pancreatic cancer

Neoadjuvant chemotherapy for pancreatic cancer: Effects on cancer tissue and novel perspectives

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