The <scp>JAK</scp>/<scp>STAT</scp>3 signalling pathway regulated angiogenesis in an endothelial cell/adipose‐derived stromal cell co‐culture, 3D gel model

Xue, Changyue; Xie, Jiamin; Zhao, Dan; Lin, Shiyu; Zhou, Tengfei; Shi, Sirong; Shao, Xin; Lin, Yunfeng; Zhu, Bofeng; Cai, Xiaoxiao

doi:10.1111/cpr.12307

Cited by 68 publications

(52 citation statements)

References 39 publications

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“…Two‐dimensional (2D) substrates with cell seeding on the surface, and three‐dimensional (3D) materials with cells encapsulated in them are currently widely used. Although 3D materials have a better spatial construction similar to the growth environment of cells in vivo, it is difficult to achieve a high degree of rigidity.…”

Section: Discussionmentioning

confidence: 99%

Stiffness regulates the proliferation and osteogenic/odontogenic differentiation of human dental pulp stem cells via the WNT signalling pathway

et al. 2018

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Section: Discussionmentioning

confidence: 99%

Stiffness regulates the proliferation and osteogenic/odontogenic differentiation of human dental pulp stem cells via the WNT signalling pathway

et al. 2018

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“…The whole cell lysis assay (KeyGen Biotech, Nanjing, China) was applied to harvest total proteins. Loading buffer was added into protein samples, as described previously (Xue et al, ). Then the mixtures were boiled at 100°C for 5 min.…”

Section: Methodsmentioning

confidence: 99%

Substrate stiffness regulated migration and angiogenesis potential of A549 cells and HUVECs

Zhao

Xue

et al. 2017

Journal Cellular Physiology

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Tumor tissue tends to stiffen during solid tumor progression. Substrate stiffness is known to alter cell behaviors, such as proliferation and migration, during which angiogenesis is requisite. Mono- and co-culture systems of lung cancer cell line A549 and human umbilical vein endothelial cells (HUVECs), on polydimethylsiloxane substrates (PDMS) with varying stiffness, were used for investigating the effects of substrate stiffness on the migration and angiogenesis of lung cancer. The expressions of matrix metalloproteinases (MMPs) and angiogenesis-related growth factors were up-regulated with the increase of substrate stiffness, whereas that of tissue inhibitor of matrix metalloproteinase (TIMPs) were down-regulated with increasing substrate stiffness. Our data not only suggested that stiff substrate may promote the migration and angiogenesis capacities of lung cancer, but also suggested that therapeutically targeting lung tumor stiffness or response of ECs to lung tumor stiffness may help reduce migration and angiogenesis of lung tumor.

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“…S2c). Since abrogation of JAK signaling may also impair angiogenesis, 35 we checked expression of the angiogenic markers Vegfα and Hif1α and evaluated numbers of cluster of differentiation 31 + vessels, but we did not observe changes upon ruxolitinib treatment (Figs. S2d and S2e).…”

Section: Jak Inhibition Impairs Human K-ras-mutated Lung Ac Cell Growmentioning

confidence: 97%

JAK–STAT inhibition impairs K‐RAS‐driven lung adenocarcinoma progression

Mohrherr

Haber

Breitenecker

et al. 2019

Intl Journal of Cancer

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Oncogenic K‐RAS has been difficult to target and currently there is no K‐RAS‐based targeted therapy available for patients suffering from K‐RAS‐driven lung adenocarcinoma (AC). Alternatively, targeting K‐RAS‐downstream effectors, K‐RAS‐cooperating signaling pathways or cancer hallmarks, such as tumor‐promoting inflammation, has been shown to be a promising therapeutic strategy. Since the JAK–STAT pathway is considered to be a central player in inflammation‐mediated tumorigenesis, we investigated here the implication of JAK–STAT signaling and the therapeutic potential of JAK1/2 inhibition in K‐RAS‐driven lung AC. Our data showed that JAK1 and JAK2 are activated in human lung AC and that increased activation of JAK–STAT signaling correlated with disease progression and K‐RAS activity in human lung AC. Accordingly, administration of the JAK1/2 selective tyrosine kinase inhibitor ruxolitinib reduced proliferation of tumor cells and effectively reduced tumor progression in immunodeficient and immunocompetent mouse models of K‐RAS‐driven lung AC. Notably, JAK1/2 inhibition led to the establishment of an antitumorigenic tumor microenvironment, characterized by decreased levels of tumor‐promoting chemokines and cytokines and reduced numbers of infiltrating myeloid derived suppressor cells, thereby impairing tumor growth. Taken together, we identified JAK1/2 inhibition as promising therapy for K‐RAS‐driven lung AC.

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The JAK/STAT3 signalling pathway regulated angiogenesis in an endothelial cell/adipose‐derived stromal cell co‐culture, 3D gel model

Cited by 68 publications

References 39 publications

Stiffness regulates the proliferation and osteogenic/odontogenic differentiation of human dental pulp stem cells via the WNT signalling pathway

Stiffness regulates the proliferation and osteogenic/odontogenic differentiation of human dental pulp stem cells via the WNT signalling pathway

Substrate stiffness regulated migration and angiogenesis potential of A549 cells and HUVECs

JAK–STAT inhibition impairs K‐RAS‐driven lung adenocarcinoma progression

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