Corrigendum: Extracellular matrix composition modulates <scp>PDAC</scp> parenchymal and stem cell plasticity and behavior through the secretome

Biondani, Giulia; Zeeberg, Katrine; Greco, Maria Raffaella; Cannone, Stefania; Dando, Ilaria; Pozza, Elisa Dalla; Mastrodonato, María; Forciniti, Stefania; Casavola, Valeria; Palmieri, Marta; Reshkin, Stephan J.; Cardone, Rosa Angela

doi:10.1111/febs.15030

Cited by 5 publications

(30 citation statements)

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“…The human pancreatic adenocarcinoma parenchymal (CPC) cell line, Panc1, and Panc1 CSCs, generated as previously described [28], were grown and maintained in standard conditions as previously described [5]. Panc1 cells express the mutated PDAC driver genes KRAS, CDKN2A, MAP2K4, and TP53 [29], [30].…”

Section: Cell Linesmentioning

confidence: 99%

“…To collect conditioned media (CM), 1.5x10 5 CAF cells/well were seeded in 24-well cell culture plates and medium changed every 3 days. When the monolayer reached approximately 80% confluence, they were incubated with 1 ml of medium with 1% FBS lacking growth factors and antibiotics for 30 hours.…”

Section: Cancer Associated Fibroblasts (Cafs)mentioning

confidence: 99%

“…Pancreatic Ductal Adenocarcinoma (PDAC) is one of the most lethal cancers having a five-year survival rate of less than 8% [1], [2] and will become the second cause of cancer deaths in the coming years [3], [4]. One of the aggressive characteristics of PDAC is their highly reactive and tumor-supportive stromal microenvironment named desmoplasia [5]. Desmoplasia is a dense extracellular matrix (ECM), which makes up to 90% of PDAC tissue [6,7] [8,9], [10] and is characterized by increasing collagen type I levels as the tumor progresses and which contains the cancer cells and their accessory cells, including cancer associated fibroblasts (CAFs) [11], [12].…”

Section: Introductionmentioning

confidence: 99%

“…Recent studies have demonstrated that the stromal ECM composition "per se" produces important cues that guide the expression of different PDAC phenotypes in both parenchymal cancer cells (CPCs) [18], [5] and CSCs [5]. In particular, ECM composition differently regulates growth, morphology, invasive, angiogenic capacities and secretome profiles in PDAC CPCs and their derived CSCs [5].…”

Section: Introductionmentioning

confidence: 99%

“…Given the complex interactions between cancer cells and CAFs, more work is needed to investigate the contributions of CAFs in enabling or maintaining hallmark behaviors in CSCs. Here, we analyzed the role of ECM collagen I in modulating the effect of CAF-derived signals with conditioned medium from primary cultured CAFs derived from patients with PDAC on the parenchymal (CPC) and CSC populations in a previously described three-dimensional (3D) organotypic model of PDAC [5] [18] mimicking the ECM of early (low collagen I levels) and late (high collagen I levels) stage PDAC tumors.…”

Section: Introductionmentioning

confidence: 99%

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The ECM and CAFs interact to differentially regulate PDAC parenchymal (CPC) and CSC phenotypes to determine pancreatic ductal adenocarcinoma (PDAC) progression

Cannone

Greco

Guizouarn³

et al. 2019

Preprint

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Section: Cell Linesmentioning

confidence: 99%

Section: Cancer Associated Fibroblasts (Cafs)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

The ECM and CAFs interact to differentially regulate PDAC parenchymal (CPC) and CSC phenotypes to determine pancreatic ductal adenocarcinoma (PDAC) progression

Cannone

Greco

Guizouarn³

et al. 2019

Preprint

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Semi‐interpenetrating polymer network cryogels based on poly(ethylene glycol) diacrylate and collagen as potential off‐the‐shelf platforms for cancer cell research

et al. 2021

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In the present work, we investigated the potential of novel semi-interpenetrating polymer network (semi-IPN) cryogels, obtained through ultraviolet exposure of aqueous mixtures of poly(ethylene glycol) diacrylate and type I collagen, as tunable offthe-shelf platforms for 3D cancer cell research. We synthesized semi-IPN cryogels with variable collagen amounts (0.1% and 1% w/v) and assessed the effect of collagen on key cryogel properties for cell culture, for example, porosity, degradation rate and mechanical stiffness. Then, we investigated the ability of the cryogels to sustain the long-term growth of two pancreatic ductal adenocarcinoma (PDAC) cell populations, the parenchymal Panc1 cells and their derived cancer stem cells. Results revealed that both cell lines efficiently infiltrated, attached and expanded in the cryogels over a period of 14 days. However, only when grown in the cryogels with the highest collagen concentration, both cell lines reproduced their characteristic growth pattern previously observed in collagen-enriched organotypic cultures, biomimetic of the highly fibrotic PDAC stroma. Cellular preembedding in Matrigel, that is, the classical approach to develop/grow organoids, interfered with an efficient intrascaffold migration and growth. Although preliminary, these findings highlight the potential of the proposed cryogels as reproducible and tunable cancer cell research platforms.

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Collagen Ⅰ-DDR1 signaling promotes hepatocellular carcinoma cell stemness via Hippo signaling repression

Xiong

Zhang

Zhu

et al. 2022

Preprint

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Background: Cancer stem cells (CSCs) are a minority population of cancer cells with stemness and multiple differentiation potentials, leading to cancer progression and therapeutic resistance. However, the concrete mechanism of CSCs remains obscure. Collagen Ⅰ-DDR1 signaling can response to ECM which can be a physical barrier that protects CSCs from chemotherapy. We explore the clinical significance, biological function and molecular mechanism of collagen Ⅰ-DDR1 signaling in promoting cancer cell stemness. Methods: Picro-Sirius red staining was performed to distinguish collagen types. We established DDR1 knock-down and overexpression in different HCC cell lines. sphere-forming assay, single-cell colony formation, CD133 positive stem-like-cell proportion, and chemoresistance was performed to assess cancer cell stemness in vitro. Cancer cells limiting dilution implantation assay was conducted to assess stemness in vivo. Stemness and Hippo signaling associated genes expression was determined by quantitative RT-PCR. Proteins interaction was investigated by mass spectrometry, co-immunoprecipitation, GST pull-down and confocal microscopy imaging. The mechanisms of collagen Ⅰ-DDR1 regulating Hippo signaling were performed by RNA sequencing, immunoprecipitation and immunoblotting. A radiomic predicting model was constructed based on T2 weighted image, the predictive performance was evaluated by receiver operating characteristic curve (ROC) analysis.Results: In advanced HCC tissues, collagen Ⅰ was upregulated, which was consistent with the expression of its receptor DDR1, high collagen Ⅰ levels accompanied by high DDR1 expression are associated with a poor prognosis in patients with HCC. Collagen Ⅰ-induced DDR1 activation enhanced HCC cell stemness in vitro and in vivo. Mechanistically, DDR1 interacts with CD44, which acts as a co-receptor that amplifies collagen Ⅰ-induced DDR1 signaling, and collagen Ⅰ-DDR1 signaling antagonized Hippo signaling by facilitating the recruitment of PP2AA to MST1, leading to exaggerated YAP activation. The combined inhibition of DDR1 and YAP synergistically abrogated HCC cell stemness. A radiomic model based on T2 weighted image can noninvasively predict collagen Ⅰ expression.Conclusions: Our findings reveal the mechanism of collagen Ⅰ-DDR1 signaling inhibiting Hippo signaling, highlight the role of CD44/DDR1/YAP axis in promoting cancer cell stemness, and the radiomic model have potential of non-invasive predicting collagen Ⅰ expression, suggesting that DDR1 and YAP may serve as novel prognostic biomarkers and therapeutic targets in HCC.

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Corrigendum: Extracellular matrix composition modulates PDAC parenchymal and stem cell plasticity and behavior through the secretome

Cited by 5 publications

References 0 publications

The ECM and CAFs interact to differentially regulate PDAC parenchymal (CPC) and CSC phenotypes to determine pancreatic ductal adenocarcinoma (PDAC) progression

The ECM and CAFs interact to differentially regulate PDAC parenchymal (CPC) and CSC phenotypes to determine pancreatic ductal adenocarcinoma (PDAC) progression

Semi‐interpenetrating polymer network cryogels based on poly(ethylene glycol) diacrylate and collagen as potential off‐the‐shelf platforms for cancer cell research

Collagen Ⅰ-DDR1 signaling promotes hepatocellular carcinoma cell stemness via Hippo signaling repression

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