Kindler syndrome protein Kindlin-1 is mainly expressed in adult tissues originating from ectoderm/endoderm

Zhan, Jun; Yang, Mei; Zhang, Jing; Guo, Yongqing; Liu, Wei; Zhang, Hongquan

doi:10.1007/s11427-014-4775-2

Cited by 6 publications

(5 citation statements)

References 27 publications

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“…Kindlin-2 (the official gene name of Kindlin-2 is FERMT2) is a focal adhesion molecule containing the conserved 4.1-ezrin-radixin-moesin (FERM) domain and is widely distributed in mesoderm-origin tissues (Zhan et al, 2015b). FERMT2 deficiency in mice is reported to cause embryonic lethality, and partial deficiency of Kindlin-2 in mice results in altered hemostasis, angiogenesis, chondrogenesis, and intracellular actin organization (Bledzka et al, 2016;Dowling et al, 2008;Montanez et al, 2008;Wu et al, 2015;Yang et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Kindlin-2 Inhibits the Hippo Signaling Pathway by Promoting Degradation of MOB1

et al. 2019

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Section: Introductionmentioning

confidence: 99%

Kindlin-2 Inhibits the Hippo Signaling Pathway by Promoting Degradation of MOB1

et al. 2019

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“…These findings indicated that both Kindlin-1 and Kindlin-2 interact with TβRI and Smad3 and activate TGF-β signaling pathway. It has also been reported that Kindlin-1 is mainly expressed in ectoderm- and endoderm-derived organs [7]. In contrast, Kindlin-2 is mainly located at mesoderm-derived organs [30].…”

Section: Discussionmentioning

confidence: 99%

“…Kindlin-1 is mainly expressed in adult tissues originating from ectoderm/endoderm [7]. Kindlin-1 was known to be essential for maintaining the structure of cell-matrix adhesion, such as focal adhesions and podosomes [8].…”

Section: Introductionmentioning

confidence: 99%

Focal adhesion molecule Kindlin-1 mediates activation of TGF-β signaling by interacting with TGF-βRI, SARA and Smad3 in colorectal cancer cells

Kong

Wang

et al. 2016

Oncotarget

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Kindlin-1, an integrin-interacting protein, has been implicated in TGF-β/Smad3 signaling. However, the molecular mechanism underlying Kindlin-1 regulation of TGF-β/Smad3 signaling remains elusive. Here, we reported that Kindlin-1 is an important mediator of TGF-β/Smad3 signaling by showing that Kindlin-1 physically interacts with TGF-β receptor I (TβRI), Smad anchor for receptor activation (SARA) and Smad3. Kindlin-1 is required for the interaction of Smad3 with TβRI, Smad3 phosphorylation, nuclear translocation, and finally the activation of TGF-β/Smad3 signaling pathway. Functionally, Kindlin-1 promoted colorectal cancer (CRC) cell proliferation in vitro and tumor growth in vivo, and was also required for CRC cell migration and invasion via an epithelial to mesenchymal transition. Kindlin-1 was found to be increased with the CRC progression from stages I to IV. Importantly, raised expression level of Kindlin-1 correlates with poor outcome in CRC patients. Taken together, we demonstrated that Kindlin-1 promotes CRC progression by recruiting SARA and Smad3 to TβRI and thereby activates TGF-β/Smad3 signaling. Thus, Kindlin-1 is a novel regulator of TGF-β/Smad3 signaling and may also be a potential target for CRC therapeutics.

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“…The complex analysis of the role of Kindlin-1 in the TGFβ pathway strongly suggests that this regulatory molecule may be a new anticancer target. Kindlin-1 is known to be essential for the maintenance of the structure of cell-matrix adhesion ( 95 ). Recently, Kindling-1 has been identified as directly interacting with the key TGFβ/SMAD3 signaling components in numerous CRC cell lines (SW1116, SW480, SW620, Caco2, HCT116, RKO, LST and HT29).…”

Section: The Characteristics Of Crc-cscs Being Considered For Csc-tarmentioning

confidence: 99%

Therapeutic strategies against cancer stem cells in human colorectal cancer (Review)

et al. 2017

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Colorectal cancer (CRC) is the third most frequent malignancy and represents the fourth most common cause of cancer-associated mortalities in the world. Despite many advances in the treatment of CRC, the 5-year survival rate of patients with CRC remains unsatisfactory due to tumor recurrence and metastases. Recently, cancer stem cells (CSCs), have been suggested to be responsible for the initiation and relapse of the disease, and have been identified in CRC. Due to their basic biological features, which include self-renewal and pluripotency, CSCs may be novel therapeutic targets for CRC and other cancer types. Conventional therapeutics only act on proliferating and mature cancer cells, while quiescent CSCs survive and often become resistant to chemotherapy. In this review, markers of CRC-CSCs are evaluated and the recently introduced experimental therapies that specifically target these cells by inducing CSC proliferation, differentiation and sensitization to apoptotic signals via molecules including Dickkopf-1, bone morphogenetic protein 4, Kindlin-1, tankyrases, and p21-activated kinase 1, are discussed. In addition, novel strategies aimed at inhibiting some crucial processes engaged in cancer progression regulated by the Wnt, transforming growth factor β and Notch signaling pathways (pyrvinium pamoate, silibinin, PRI-724, P17, and P144 peptides) are also evaluated. Although the metabolic alterations in cancer were first described decades ago, it is only recently that the concept of targeting key regulatory molecules of cell metabolism, such as sirtuin 1 (miR-34a) and AMPK (metformin), has emerged. In conclusion, the discovery of CSCs has resulted in the definition of novel therapeutic targets and the development of novel experimental therapies for CRC. However, further investigations are required in order to apply these novel drugs in human CRC.

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Kindler syndrome protein Kindlin-1 is mainly expressed in adult tissues originating from ectoderm/endoderm

Cited by 6 publications

References 27 publications

Kindlin-2 Inhibits the Hippo Signaling Pathway by Promoting Degradation of MOB1

Kindlin-2 Inhibits the Hippo Signaling Pathway by Promoting Degradation of MOB1

Focal adhesion molecule Kindlin-1 mediates activation of TGF-β signaling by interacting with TGF-βRI, SARA and Smad3 in colorectal cancer cells

Therapeutic strategies against cancer stem cells in human colorectal cancer (Review)

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