A panel of four genes accurately differentiates benign from malignant thyroid nodules

Wang, Qingxuan; Chen, Endong; Cai, Yefeng; Li, Quan; Jin, Yi-Xiang; Jin, Weiwei; Wang, Ying-Hao; Zheng, Zhouci; Xue, Lu; Wang, Ouchen; Zhang, Xiaohua

doi:10.1186/s13046-016-0447-3

Cited by 30 publications

(27 citation statements)

References 45 publications

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“…With the help of sequencing technology, we have been revealed whole transcriptome bioinformation of 19 pairs PTC samples and its adjacent normal thyroid tissues . The results showed that SCARA5 might act as a vital anti‐tumour gene in the PTC.…”

Section: Introductionmentioning

confidence: 99%

Scavenger receptor class A, member 5 is associated with thyroid cancer cell lines progression via epithelial‐mesenchymal transition

Zheng

Xia

Quan

et al. 2020

Cell Biochemistry & Function

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Thyroid cancer (TC) has become one of most common endocrine malignancies in recent decades. Due to gene background polymorphism, it's outcome goes quite differently in each patient. For exploring the mechanism, we performed whole transcriptome sequencing of paired papillary thyroid carcinoma (PTC) and adjacent thyroid tissues. As a result, scavenger receptor class A member 5 (SCARA5) might be a crucial anti-oncogene associated with PTC. By RT-qPCR, we first detected the expression of SCARA5 in PTC tissue and three type of TC cell lines. Besides, The Cancer Genome Atlas (TCGA) data were gathered to analysis the relationship between SCARA5 and clinical feature. A series of loss-function experiments in TC cell lines (KTC-1 and BCPAP) to investigate the function of SCARA5 in PTC. The results showed that SCARA5 expression in PTC was lower than adjacent normal tissue. And, it's consistent with the TCGA database. After analyse the correlation between SCARA5 expression and clinicopathological features in TCGA database, we discovered that downregulated SCARA5 is significantly connected age (P = .04) and tumour size (P = .032). Knockdown of SCARA5 in TC cell line could significantly increase the function of cells proliferation, colony formation, migration, and invasion. Furthermore, we also proved that SCARA5 could modulate the expression of epithelial-mesenchymal transition-related proteins, which influence invasion and migration. To best of our knowledge, SCARA5 is a suppressor gene which was associated with PTC and might be a potential therapeutic target in the future.Significance of the study: Thyroid cancer (TC) has become one of most common endocrine malignancies in recent decades. By whole transcriptome sequencing of paired papillary thyroid carcinoma (PTC) and adjacent thyroid tissues, author discovered that scavenger receptor class A member 5 (SCARA5) might be crucial antioncogene associated with PTC. Furthermore, knocking-down of SCARA5 in TC cell line can increase the function of cells proliferation, colony formation, migration, and invasion. Author also proved that SCARA5 could modulate the expression of epithelialmesenchymal transition-related proteins.Ru-Tian Hao and Ou-Chen Wang contributed equally to this study.

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Section: Introductionmentioning

confidence: 99%

Scavenger receptor class A, member 5 is associated with thyroid cancer cell lines progression via epithelial‐mesenchymal transition

Zheng

Xia

Quan

et al. 2020

Cell Biochemistry & Function

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“…Next‐generation sequencing has been widely used in the study of the gene expression variations and cancer molecular mechanism. In our previous study, we selected 19 matched pairs of thyroid carcinoma tissues and nearby non‐cancerous tissues and the outcomes revealed that GAP43 expression was overexpressed in tumour tissues. This finding suggested GAP43 may have a possible role as an oncogene in PTC.…”

Section: Discussionmentioning

confidence: 99%

“…In our previous study, we have conducted next‐generation of 19 pairs of PTC tissues and adjacent normal thyroid tissue . After evaluating all the information, we identified that growth‐associated protein 43 (GAP43), a gene encoding an axonal membrane protein, as an oncogene promotes PTC tumorigenesis and tumour progression . As for the normal function of this protein, it is normally expressed in neuronal somata, axons and growth cones during pre‐ and early postnatal development .…”

Section: Introductionmentioning

confidence: 99%

“…19 After evaluating all the information, we identified that growth-associated protein 43 (GAP43), a gene encoding an axonal membrane protein, as an oncogene promotes PTC tumorigenesis and tumour progression. 19 As for the normal function of this protein, it is normally expressed in neuronal somata, axons and growth cones during pre-and early postnatal development. 20,21 Consistently, it also plays a fundamental function in neural growth, axonal regeneration and stabilisation of synaptic function.…”

Section: Introductionmentioning

confidence: 99%

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Growth‐associated protein 43 promotes thyroid cancer cell lines progression via epithelial‐mesenchymal transition

Zheng

Quan

et al. 2019

J Cellular Molecular Medi

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Thyroid cancer is maintaining at a high incidence level and its carcinogenesis is mainly affected by a complex gene interaction. By analysis of the next‐generation resequencing of paired papillary thyroid cancer (PTC) and adjacent thyroid tissues, we found that Growth Associated Protein 43 (GAP43), a phosphoprotein activated by protein kinase C, might be novel markers associated with PTC. However, its function in thyroid carcinoma has been poorly understood. We discovered that GAP43 was significantly overexpressed in thyroid carcinoma and these results were consistent with that in The Cancer Genome Atlas (TCGA) cohort. In addition, some clinicopathological features of GAP43 in TCGA database showed that up‐regulated GAP43 is significantly connected to lymph node metastasis (P < 0.001) and tumour size (P = 0.038). In vitro experiments, loss of function experiments was performed to investigate GAP43 in PTC cell lines (TPC‐1 and BCPAP). The results proved that GAP43 knockdown in PTC cell significantly decreased the function of cell proliferation, colony formation, migration, and invasion and induced cell apoptosis. Furthermore, we also indicated that GAP43 could modulate the expression of epithelial‐mesenchymal transition‐related proteins, which could influence invasion and migration. Put those results together, GAP43 is a gene which was associated with PTC and might be a potential therapeutic target.

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“…Other technologies, including gene and protein expression signatures [210][211][212][213][214], have also been developed to help to decipher the code that differentiates benign and cancerous molecular anomalies. Intriguingly, there are models that predict (with up to 90% accuracy) the pattern of epigenetic changes found on circulating DNA in the bloodstream that imply malignancy versus those that do not [215].…”

Section: Confounding the Holy Grail-early Detection Of Cancer With Blmentioning

confidence: 99%

The paradox of cancer genes in non-malignant conditions: implications for precision medicine

et al. 2020

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Next-generation sequencing has enabled patient selection for targeted drugs, some of which have shown remarkable efficacy in cancers that have the cognate molecular signatures. Intriguingly, rapidly emerging data indicate that altered genes representing oncogenic drivers can also be found in sporadic non-malignant conditions, some of which have negligible and/or low potential for transformation to cancer. For instance, activating KRAS mutations are discerned in endometriosis and in brain arteriovenous malformations, inactivating TP53 tumor suppressor mutations in rheumatoid arthritis synovium, and AKT, MAPK, and AMPK pathway gene alterations in the brains of Alzheimer's disease patients. Furthermore, these types of alterations may also characterize hereditary conditions that result in diverse disabilities and that are associated with a range of lifetime susceptibility to the development of cancer, varying from near universal to no elevated risk. Very recently, the repurposing of targeted cancer drugs for non-malignant conditions that are associated with these genomic alterations has yielded therapeutic successes. For instance, the phenotypic manifestations of CLOVES syndrome, which is characterized by tissue overgrowth and complex vascular anomalies that result from the activation of PIK3CA mutations, can be ameliorated by the PIK3CA inhibitor alpelisib, which was developed and approved for breast cancer. In this review, we discuss the profound implications of finding molecular alterations in non-malignant conditions that are indistinguishable from those driving cancers, with respect to our understanding of the genomic basis of medicine, the potential confounding effects in early cancer detection that relies on sensitive blood tests for oncogenic mutations, and the possibility of reverse repurposing drugs that are used in oncology in order to ameliorate nonmalignant illnesses and/or to prevent the emergence of cancer.

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A panel of four genes accurately differentiates benign from malignant thyroid nodules

Cited by 30 publications

References 45 publications

Scavenger receptor class A, member 5 is associated with thyroid cancer cell lines progression via epithelial‐mesenchymal transition

Scavenger receptor class A, member 5 is associated with thyroid cancer cell lines progression via epithelial‐mesenchymal transition

Growth‐associated protein 43 promotes thyroid cancer cell lines progression via epithelial‐mesenchymal transition

The paradox of cancer genes in non-malignant conditions: implications for precision medicine

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