Advanced mechanotherapy: Biotensegrity  for governing metastatic tumor cell fate via modulating the extracellular matrix

Abdollahiyan, Parinaz; Oroojalian, Fatemeh; Baradaran, Behzad; Guárdia, Miguel de la; Mokhtarzadeh, Ahad

doi:10.1016/j.jconrel.2021.06.002

Cited by 11 publications

(6 citation statements)

References 252 publications

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“…The role of mechanical forces in cancer has now become clear and sparked the idea of using the physical properties of TME in a targeted manner [ 498 ]. Several clinical studies with ECM-normalizing drugs and drugs that target mechanotransduction with a possible effect on MMP-14 function are currently underway [ 498 , 499 ]. Targeting transglutaminase or lysyl oxidase with therapeutics could be options to fight cancer by reversing the biomechanical stiffening of the TME [ 456 , 457 ].…”

Section: Translational Perspectives: Mmps and Invadopodia Are Worthwhile Targets For Inhibiting Cancer Progressionmentioning

confidence: 99%

Matrix Metalloproteinases Shape the Tumor Microenvironment in Cancer Progression

Niland

Riscanevo

Eble

2021

IJMS

221

107

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Cancer progression with uncontrolled tumor growth, local invasion, and metastasis depends largely on the proteolytic activity of numerous matrix metalloproteinases (MMPs), which affect tissue integrity, immune cell recruitment, and tissue turnover by degrading extracellular matrix (ECM) components and by releasing matrikines, cell surface-bound cytokines, growth factors, or their receptors. Among the MMPs, MMP-14 is the driving force behind extracellular matrix and tissue destruction during cancer invasion and metastasis. MMP-14 also influences both intercellular as well as cell–matrix communication by regulating the activity of many plasma membrane-anchored and extracellular proteins. Cancer cells and other cells of the tumor stroma, embedded in a common extracellular matrix, interact with their matrix by means of various adhesive structures, of which particularly invadopodia are capable to remodel the matrix through spatially and temporally finely tuned proteolysis. As a deeper understanding of the underlying functional mechanisms is beneficial for the development of new prognostic and predictive markers and for targeted therapies, this review examined the current knowledge of the interplay of the various MMPs in the cancer context on the protein, subcellular, and cellular level with a focus on MMP14.

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Section: Translational Perspectives: Mmps and Invadopodia Are Worthwhile Targets For Inhibiting Cancer Progressionmentioning

confidence: 99%

Matrix Metalloproteinases Shape the Tumor Microenvironment in Cancer Progression

Niland

Riscanevo

Eble

2021

IJMS

221

107

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“…Several studies have identified YAP as a transductor of ECM stiffness signals. 25 , 26 Hence, we conducted the current research to investigate whether YAP can sense the bladder ECM stiffness changes. hBdSMCs were cultured on “soft” (0.5 kPa) and “stiff” (32 kPa) gels for 24 h. hBdSMCs were infected with adeno‐associated virus (AAV) containing YAP shRNA and overexpression vector with GFP green fluorescence.…”

Section: Resultsmentioning

confidence: 99%

“…The transcription coactivator YAP plays a vital role in tissue and organ development and regeneration. Several studies have identified YAP as a transductor of ECM stiffness signals 25,26 . Hence, we conducted the current research to investigate whether YAP can sense the bladder ECM stiffness changes.…”

Section: Resultsmentioning

confidence: 99%

YAP/Smad3 promotes pathological extracellular matrix microenviroment‐induced bladder smooth muscle proliferation in bladder fibrosis progression

Jin

et al. 2022

MedComm

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Fibrosis is a chronic inflammation process with excess extracellular matrix (ECM) deposition that cannot be reversed. Patients suffer from bladder dysfunction caused by bladder fibrosis. Moreover, the interactive mechanisms between ECM and bladder fibrosis are still obscure. Hence, we assessed the pivotal effect of Yes‐associated protein (YAP) on the proliferation of bladder smooth muscle in fibrosis process. We identified that stiff ECM increased the expression and translocation of YAP in the nucleus of human bladder smooth muscle cell (hBdSMC). Sequencings and proteomics revealed that YAP bound to Smad3 and promoted the proliferation of hBdSMC via MAPK/ERK signaling pathway in stiff ECM. Moreover, CUT and TAG sequencing and dual‐luciferase assays demonstrated that Smad3 inhibited the transcription of JUN. The YAP inhibitor CA3 was used in a partial bladder outlet obstruction (pBOO) rat model. The results showed that CA3 attenuated bladder smooth muscle proliferation. Collectively, YAP binding with Smad3 in the nucleus inhibited the transcription of JUN, and promoted the proliferation of bladder smooth muscle through the MAPK/ERK signaling pathway. The current study identified a novel mechanism of mechanical force induced bladder fibrosis that provided insights in YAP‐associated organ fibrosis.

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“…However, studies on the process by which the mechanotransduction of is related to the vascular system are just emerging ( 17 ). The Hippo signaling pathway has two associated transcriptional co-activators, YES-associated protein 1 (YAP) and TAZ (or WWRT1), which are activated by the ECM and thus serve as a central regulator of cell proliferation, which can regulate the growth and development of tissue ( 94 , 95 ). It was found that pulmonary vascular stiffness can activate YAP/TAZ at early PH, thus inducing the Mir-130/301 family to further enhance ECM remodeling and cell proliferation in vivo ( 96 , 97 ).…”

Section: Glutamine Metabolism In Pulmonary Hypertensionmentioning

confidence: 99%

The Role of Glutamine and Glutaminase in Pulmonary Hypertension

Wang

et al. 2022

Front. Cardiovasc. Med.

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Pulmonary hypertension (PH) refers to a clinical and pathophysiological syndrome in which pulmonary vascular resistance and pulmonary arterial pressure are increased due to structural or functional changes in pulmonary vasculature caused by a variety of etiologies and different pathogenic mechanisms. It is followed by the development of right heart failure and even death. In recent years, most studies have found that PH and cancer shared a complex common pathological metabolic disturbance, such as the shift from oxidative phosphorylation to glycolysis. During the shifting process, there is an upregulation of glutamine decomposition driven by glutaminase. However, the relationship between PH and glutamine hydrolysis, especially by glutaminase is yet unclear. This review aims to explore the special linking among glutamine hydrolysis, glutaminase and PH, so as to provide theoretical basis for clinical precision treatment in PH.

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Advanced mechanotherapy: Biotensegrity for governing metastatic tumor cell fate via modulating the extracellular matrix

Cited by 11 publications

References 252 publications

Matrix Metalloproteinases Shape the Tumor Microenvironment in Cancer Progression

Matrix Metalloproteinases Shape the Tumor Microenvironment in Cancer Progression

YAP/Smad3 promotes pathological extracellular matrix microenviroment‐induced bladder smooth muscle proliferation in bladder fibrosis progression

The Role of Glutamine and Glutaminase in Pulmonary Hypertension

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