Growth factor receptor bound protein-7 regulates proliferation, cell cycle, and mitochondrial apoptosis of thyroid cance
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Growth factor receptor bound protein‑7 regulates proliferation, cell cycle, and mitochondrial apoptosis of thyroid cancer cells via MAPK/ ERK signaling Haili Tang1 · Ping Yang1 · Xiaojun Yang1 · Shujia Peng1 · Xi’e Hu1 · Guoqiang Bao1 Received: 10 December 2019 / Accepted: 15 June 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract It is of great significance to explore the molecular mechanism of thyroid cancer (TC) pathogenesis for its improvement and therapy. Growth factor receptor bound protein-7 (GRB7) has been regarded as an important regulatory gene in the developments of various malignant tumors. Our study aimed to illustrate the role of GRB7 in the TC pathology mechanism. Firstly, GRB7 was found to be significantly upregulated in 49 cases of TC tissues and 5 TC cell lines by using real-time quantitative polymerase chain reaction (RT-qPCR) and western blotting. Silencing GRB7 with siRNA dramatically inhibited proliferation and induced cell cycle arrest in TC cells. Besides, GRB7 silence resulted in the decrease of adenosine triphosphate content, glucose uptake, and lactose production in TC cells and attenuated the activity and expression of mitochondrial respiratory complex. We also demonstrated that GRB7 downregulation increased the levels of Bax and caspase 3, and inhibited the expression of Bcl-2, suggesting the induced mitochondrial apoptosis. More importantly, our study proved that mitogenactivated protein kinase/extracellular-regulated protein kinases (MAPK/ERK) signaling played a crucial role in the regulation of GRB7 on TC cell functions. In general, the present research verified that GRB7 was upregulated during TC development and modulated the proliferation, cell cycle, and mitochondrial apoptosis of TC cells by activating MAPK/ERK pathway. This may provide a novel target for the therapeutic strategy of TC. Keywords GRB7 · Thyroid cancer · Mitochondrial apoptosis · Proliferation · MAPK/ERK signaling
Introduction Originating from the thyroid follicle or parafollicular cells, thyroid cancer (TC) is a common malignant cancer associated with the endocrine system [1]. In the past decades, the incidence and mortality of TC have been gradually increasing [2]. Besides, TC is a typical chronic disease which constantly afflicts patients and pushes them to long-term monitoring or medication [3]. The need for further effective Haili Tang and Ping Yang have contributed equally to this work. Electronic supplementary material The online version of this article (https://doi.org/10.1007/s11010-020-03798-4) contains supplementary material, which is available to authorized users. * Guoqiang Bao [email protected] 1
Department of General Surgery, Tangdu Hospital Fourth Military Medical University, 569 Xinsi Road, Xi’an 710032, China
strategies of TC diagnosis and therapy is urgently required due to its high recurrence [4]. Therefore, exploring pivotal regulatory genes in the pathological process of TC is still a hot research topic. At present, multiple malignant tumors are u
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