GABA Receptor Expression in Benign and Malignant Thyroid Tumors

Roberts, Stephen S.; Mendonca-Torres, Maria Cecilia; Jensen, Kirk; Francis, Gary L.; Vasko, Vasyl

doi:10.1007/s12253-009-9165-x

Cited by 29 publications

(31 citation statements)

References 23 publications

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“…Baclofen could inhibit human HCC cell growth 39. GABBR also has been reported to be upregulated in thyroid cancer tissues when compared with the corresponding normal tissues 40. In our study, we found that miR‐106a/b, miR‐20a/b, and miR‐17 directly targeted the same site of the GABBR1 3′UTR in colorectal cancer.…”

Section: Discussionsupporting

confidence: 51%

A miRNAs panel promotes the proliferation and invasion of colorectal cancer cells by targeting GABBR1

et al. 2016

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MicroRNAs (miRNAs) have been implicated in the regulation of colorectal cancer. Despite the expression of miR‐17‐92 cluster in cancer has been gradually revealed, the role of each individual miRNAs in colorectal cancer still remains unclear. We studied the impact of miR‐106a/b, miR‐20a/b, and miR‐17 of miR‐17‐92 cluster on colorectal cancer cells. Real‐time quantitative polymerase chain reactions (RT‐PCR) were used to test these five miRNAs expression in colorectal cancer cell line HCT116. 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2‐H‐tetrazolium bromide (MTT) assays, Bromodeoxyuridine (BrdU), and Transwell invasion assays were used to explore the effects of these five miRNAs in colorectal cancer cells. Luciferase reporter assay, RT‐PCR, and western blotting were performed to validate the interaction of these five miRNAs with the gamma‐amino‐butyric acid type B receptor 1(GABBR1). We found that these five miRNAs were significantly upregulated in colorectal cancer samples compared with normal tissues. Forced expression of these five miRNAs significantly promoted HCT116 and HT‐29 cells proliferation and invasion. We further found that these five miRNAs function as oncogenes in colorectal cancer by specifically binding to the 3‐untranslated regions (3′UTR) of GABBR1.Furthermore, inhibition of GABBR1 could mimic the function of miRNAs in HCT116 cells, while overexpression of GABBR1 blocked the function of miRNAs‐promoted proliferation and invasion. In conclusion, miR‐106a/b, miR‐20a/b, and miR‐17 contribute to the proliferation and invasion of colorectal cancer by targeting their common target gene, GABBR1, and played a critical role in the proliferation and invasion of colorectal cancer.

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Section: Discussionsupporting

confidence: 51%

A miRNAs panel promotes the proliferation and invasion of colorectal cancer cells by targeting GABBR1

et al. 2016

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“…Importantly, the expression level of GABA B receptors was upregulated in some human tumor tissues when compared with the corresponding normal tissues. Roberts et al (2009) in human ductal breast cancer (six cases) by immunohistochemistry, and the preliminary data (Fig. 3) showed that GABA B1 expression was significantly higher in malignant …”

Section: Receptors and Tumor Developmentmentioning

confidence: 80%

GABA_B Receptor Complex as a Potential Target for Tumor Therapy

Jiang

Zhang

et al. 2012

J Histochem Cytochem.

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γ-Aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the vertebrate central nervous system. Metabotropic GABAB receptors are heterodimeric G-protein-coupled receptors (GPCRs) consisting of GABAB1 and GABAB2 subunits. The intracellular C-terminal domains of GABAB receptors are involved in heterodimerization, oligomerization, and association with other proteins, which results in a large receptor complex. Multiple splice variants of the GABAB1 subunit have been identified in which GABAB1a and GABAB1b are the most abundant isoforms in the nervous system. Isoforms GABAB1c through GABAB1n are minor isoforms and are detectable only at mRNA levels. Some of the minor isoforms have been detected in peripheral tissues and encode putative soluble proteins with C-terminal truncations. Interestingly, increased expression of GABAB receptors has been detected in several human cancer cells and tissues. Moreover, GABAB receptor agonist baclofen inhibited tumor growth in rat models. GABAB receptor activation not only induces suppressing the proliferation and migration of various human tumor cells but also results in inactivation of CREB (cAMP-responsive element binding protein) and ERK in tumor cells. Their structural complexity makes it possible to disrupt the functions of GABAB receptors in various ways, raising GABAB receptor diversity as a potential therapeutic target in some human cancers.

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“…In addition, GABARAP/GATE-16 members function in intracellular protein trafficking (93). Expression profiling of a GABARAP family member (GABARAP) was performed in human tumor specimens (without investigation of a direct link to autophagy) of thyroid cancer (94) and CRC [where GABARAP protein was overexpressed compared with matched, adjacent normal tissue (95)], and breast cancer [where both mRNA and protein levels for GABARAP were reduced (although they were not assessed in the same sample) compared with nonmatched, normal breast tissue (96)]. Future classification of GABARAP/GATE-16 proteins with respect to autophagy-specific function may reveal additional targets for IHC assessment of autophagy status in tumors.…”

Section: Tumor-related Mrna and Protein Alterations Of Map1lc3 And Itmentioning

confidence: 99%

Here, There Be Dragons: Charting Autophagy-Related Alterations in Human Tumors

Lebovitz

Bortnik

Gorski

2012

Clinical Cancer Research

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Macroautophagy (or autophagy) is a catabolic cellular process that is both homeostatic and stress adaptive. Normal cells rely on basal levels of autophagy to maintain cellular integrity (via turnover of longlived proteins and damaged organelles) and increased levels of autophagy to buoy cell survival during various metabolic stresses (via nutrient and energy provision through lysosomal degradation of cytoplasmic components). Autophagy can function in both tumor suppression and tumor progression, and is under investigation in clinical trials as a novel target for anticancer therapy. However, its role in cancer pathogenesis has yet to be fully explored. In particular, it remains unknown whether in vitro observations will be applicable to human cancer patients. Another outstanding question is whether there exists tumorspecific selection for alterations in autophagy function. In this review, we survey reported mutations in autophagy genes and key autophagy regulators identified in human tumor samples and summarize the literature regarding expression levels of autophagy genes and proteins in various cancer tissues. Although it is too early to draw inferences from this collection of in vivo studies of autophagy-related alterations in human cancers, their results highlight the challenges that must be overcome before we can accurately assess the scope of autophagy's predicted role in tumorigenesis.

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GABA Receptor Expression in Benign and Malignant Thyroid Tumors

Cited by 29 publications

References 23 publications

A miRNAs panel promotes the proliferation and invasion of colorectal cancer cells by targeting GABBR1

A miRNAs panel promotes the proliferation and invasion of colorectal cancer cells by targeting GABBR1

GABA_B Receptor Complex as a Potential Target for Tumor Therapy

Here, There Be Dragons: Charting Autophagy-Related Alterations in Human Tumors

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GABA Receptor Expression in Benign and Malignant Thyroid Tumors

Cited by 29 publications

References 23 publications

A miRNAs panel promotes the proliferation and invasion of colorectal cancer cells by targeting GABBR1

A miRNAs panel promotes the proliferation and invasion of colorectal cancer cells by targeting GABBR1

GABAB Receptor Complex as a Potential Target for Tumor Therapy

Here, There Be Dragons: Charting Autophagy-Related Alterations in Human Tumors

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GABA_B Receptor Complex as a Potential Target for Tumor Therapy