Tenascin-C at a glance

Midwood, Kim S.; Chiquet, Matthias; Tucker, Richard P.; Orend, Gertraud

doi:10.1242/jcs.190546

Cited by 358 publications

(388 citation statements)

References 97 publications

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“…In several compounds currently in clinical trials, antibodies against Tnc have been conjugated to either radioactive compounds that can inhibit tumor growth or IL-2, aimed at improving the efficacy of chemotherapy. Another area showing promise is the development of therapeutic or preventive cancer vaccines in which Tnc could be targeted alone or in combination with other factors (41).…”

Section: Discussionmentioning

confidence: 99%

Quantitative proteomics identify Tenascin-C as a promoter of lung cancer progression and contributor to a signature prognostic of patient survival

Gocheva

Naba

Bhutkar

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

124

130

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The extracellular microenvironment is an integral component of normal and diseased tissues that is poorly understood owing to its complexity. To investigate the contribution of the microenvironment to lung fibrosis and adenocarcinoma progression, two pathologies characterized by excessive stromal expansion, we used mouse models to characterize the extracellular matrix (ECM) composition of normal lung, fibrotic lung, lung tumors, and metastases. Using quantitative proteomics, we identified and assayed the abundance of 113 ECM proteins, which revealed robust ECM protein signatures unique to fibrosis, primary tumors, or metastases. These analyses indicated significantly increased abundance of several S100 proteins, including Fibronectin and Tenascin-C (Tnc), in primary lung tumors and associated lymph node metastases compared with normal tissue. We further showed that Tnc expression is repressed by the transcription factor Nkx2-1, a well-established suppressor of metastatic progression. We found that increasing the levels of Tnc, via CRISPR-mediated transcriptional activation of the endogenous gene, enhanced the metastatic dissemination of lung adenocarcinoma cells. Interrogation of human cancer gene expression data revealed that high TNC expression correlates with worse prognosis for lung adenocarcinoma, and that a three-gene expression signature comprising TNC, S100A10, and S100A11 is a robust predictor of patient survival independent of age, sex, smoking history, and mutational load. Our findings suggest that the poorly understood ECM composition of the fibrotic and tumor microenvironment is an underexplored source of diagnostic markers and potential therapeutic targets for cancer patients.

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Section: Discussionmentioning

confidence: 99%

Quantitative proteomics identify Tenascin-C as a promoter of lung cancer progression and contributor to a signature prognostic of patient survival

Gocheva

Naba

Bhutkar

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

124

130

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“…HER2 amplification and hyperactivation drive the growth and survival of cancers through the activation of signaling pathways including RAS/MAPK. Tenascin‐C is an extracellular matrix glycoprotein and is highly expressed during embryonic development, wound healing, inflammation, and cancer invasion . It is a crucial molecule in controlling cellular activity in adaptation during normal vascular development as well as tissue remodeling.…”

Section: Discussionmentioning

confidence: 93%

Potential biomarkers of kaposiform lymphangiomatosis

Ozeki

Nozawa

Kawamoto

et al. 2019

Pediatric Blood & Cancer

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Background Kaposiform lymphangiomatosis (KLA) has recently been distinguished as a novel subtype of generalized lymphatic anomaly (GLA), and is characterized by foci of spindle endothelial cells amid a background of malformed lymphatic channels. The etiology of these diseases remains unknown and diagnosis is confounded by their similar clinical findings. This study aimed to clarify differences in the clinical findings and plasma cytokine profiles of GLA and KLA patients. Procedure Clinical features data of GLA and KLA patients were obtained from a national survey. Differences in clinical findings, plasma levels of cytokines, and survival were analyzed. Plasma was obtained from healthy controls and GLA and KLA patients. Thirty‐six angiogenic and lymphangiogenic factors were evaluated for cytokine concentration. Results Twenty‐one patients with GLA and 11 with KLA were recruited. Mediastinal masses, hemorrhagic pericardial and pleural effusion, coagulation disorders, and thrombocytopenia were more frequent in KLA than in GLA. KLA had a significantly poorer outcome than GLA (P = 0.044). Soluble VEGFR3, angiopoietin 2, HGF, soluble HER2, tenascin C, and soluble HGFR levels were higher in KLA. Notably, soluble VEGFR3 and angiopoietin 2 levels were approximately 10‐fold higher than those of other molecules measured. However, soluble VEGFR1 and soluble TIE2 were lower in KLA than in GLA and the controls. Conclusions Patients with KLA have an unfavorable prognosis and serious symptoms (hemorrhagic pleural effusion and coagulation disorders). Our data indicate that eight angiogenic cytokines might be potential biomarkers of KLA.

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“…Обнаружено, что тенасцин специфически индуцируется в макрофагах и миелоцитах при патогенной инфекции и / или повре-ждении тканей, а также при развитии опухолевых про-цессов, и в свою очередь индуцирует продукцию miR-155 (рис. 2) [28,29]. Группой исследователей из США, Франции и Ита-лии опубликована целая серия экспериментальных ра-бот и обзоров, посвященных участию miR-155 в регуля-ции иммунных реакций в норме и при патологии [8,21,24,30,31].…”

Section: иммунологические реакции и Mir-155unclassified

“…В данном обзоре мы не затрагиваем участия тенас-цина и QKI в возникновении и прогрессии гемоблас-тозов и солидных опухолей, хотя эта тема сейчас ак-тивно обсуждается в мировой литературе [29,32]. На наш взгляд, роль этих белков в канцерогенезе за-служивает особого внимания, однако в большой сте-пени она связана с функционированием иммунной системы.…”

Section: солидные опухоли и Mir-155unclassified

MicroRNA-155-5p in pathogenesis of cancer

Зборовская¹,

Komelkov²

2017

Usp. mol. onkol

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ВведениеМикроРНК -класс малых (18-25 нуклеотидов) РНК, регулирующих экспрессию генов на посттран-скрипционном уровне. Число работ, посвященных исследованиям микроРНК при различных заболева-ниях человека, особенно онкологических, неуклонно растет. Однако, несмотря на усилия в изучении меха-низмов действия различных микроРНК, их прямого или опосредованного участия в модулировании кле-точных сигнальных путей и определения роли в про-цессах опухолевого роста, картина все более усложняет-ся. Проблема заключается, в первую очередь, в том, что большинство микроРНК многофункциональны, регулируют экспрессию сразу нескольких генов, при том, что один и тот же ген может посттранскрип-ционно регулироваться сразу несколькими микроРНК. В разных клеточных типах и даже в пределах схожих клеточных контекстов одна и та же микроРНК высту-пает в роли то онкогена, то опухолевого супрессора [1,2]. Эти утверждения прекрасно иллюстрирует рабо-та исследователей из Онкологического центра Андер-сона (Anderson Cancer Center, Техас) и Кэмбриджского университета (University of Cambridge, Кембридж), опубликованная в 2015 г. в журнале, аффилированном с Nature [3]. Авторы дали подробную и хорошо аргу-ментированную характеристику отдельным микроРНК и их кластерам, ассоциированным с целым рядом кле-точных процессов и сигнальных путей, и попытались

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Tenascin-C at a glance

Cited by 358 publications

References 97 publications

Quantitative proteomics identify Tenascin-C as a promoter of lung cancer progression and contributor to a signature prognostic of patient survival

Quantitative proteomics identify Tenascin-C as a promoter of lung cancer progression and contributor to a signature prognostic of patient survival

Potential biomarkers of kaposiform lymphangiomatosis

MicroRNA-155-5p in pathogenesis of cancer

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