lncRNA SNHG3 acts as a novel Tumor Suppressor and regulates Tumor Proliferation and Metastasis via AKT/mTOR/ERK pathway in Papillary Thyroid Carcinoma

Duan, Yu; Wang, Zhiyong; Xu, Lijuan; Sun, Li; Song, Hairong; Yin, Hang; He, Fucheng

doi:10.7150/jca.42070

Cited by 32 publications

(29 citation statements)

References 31 publications

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“…These results suggest that SNHG3 may be a diagnostic and therapeutic target for PTC. Duan et al [ 77 ] found that lncRNA SNHG3 was significantly downregulated in PTC tissues and cell lines. Functional studies have shown that SNHG3 deletion promotes the proliferation, migration and invasion of PTC cells.…”

Section: Lncrna Snhg3 Dysregulation In Human Cancersmentioning

confidence: 99%

LncRNA SNHG3, a potential oncogene in human cancers

Mei

et al. 2020

Cancer Cell Int

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Long noncoding RNAs (lncRNAs) are composed of > 200 nucleotides; they lack the ability to encode proteins but play important roles in a variety of human tumors. A large number of studies have shown that dysregulated expression of lncRNAs is related to tumor oncogenesis and progression. Emerging evidence shows that SNHG3 is a novel oncogenic lncRNA that is abnormally expressed in various tumors, including osteosarcoma, liver cancer, lung cancer, etc. SNHG3 primarily competes as a competitive endogenous RNA (ceRNA) that targets tumor suppressor microRNAs (miRNAs) and ceRNA mechanisms that regulate biological processes of tumors. In addition, abnormal expression of SNHG3 is significantly correlated with patient clinical features. Upregulation of SNHG3 contributes to biological functions, including tumor cell proliferation, migration, invasion and EMT. Therefore, SNHG3 may represent a potential diagnostic and prognostic biomarker, as well as a novel therapeutic target.

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Section: Lncrna Snhg3 Dysregulation In Human Cancersmentioning

confidence: 99%

LncRNA SNHG3, a potential oncogene in human cancers

Mei

et al. 2020

Cancer Cell Int

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“…Cell growth rate was detected by using commercial Cell Counting Kit-8 reagent as previously described [21]. CRC cells at a density of 1×10 3 per well were seeded into a 96-well plate with ve repeats.…”

Section: Cell Proliferation and Colony Formation Assaymentioning

confidence: 99%

Aberrant SLC6A14 Expression Promotes Proliferation and Metastasis of Colorectal Cancer Via Enhancing the JAK2/STAT3 Pathway

Mao

Sheng

Jia

et al. 2020

Preprint

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Background: Solute carrier family 6 member 14 (SLC6A14) is a high-capacity amino acid transporter in mammalian cells. It has gained increasing attention for its potential involvement in the progression and metabolic reprogramming of various malignant tumors. However, the role of SLC6A14 in colorectal cancer (CRC) remains unclear. Methods: Real-time polymerase chain reaction (qRT-PCR), immunoblotting and immunohistochemistry were carried out to detect the expression level of SLC6A14 in human CRC tissues and CRC-derived cell lines. HCT-116 and Caco-2 cell lines were selected to conduct the in vitro functional studies. Cell Counting Kit-8 (CCK-8), colony formation, flow cytometry, cell migration and invasion assays were performed to investigate the role of SLC6A14 in CRC cells. Besides, Azoxymethane/Dextran Sulfate Sodium Salt (AOM/DSS)-induced CRC and tumor xenograft models were constructed to explore the effects of SLC6A14 blockade or overexpression on tumor progression in vivo. Results: SLC6A14 was substantially increased in human CRC samples and higher levels of SLC6A14 was correlated with advanced tumor stage, lymph node metastasis and dismal survival of CRC patients. SLC6A14 markedly promoted cell growth, inhibited cell apoptosis, exacerbated migration and invasion of CRC cells in vitro. Mechanistically, SLC6A14 aggravated these malignant phenotypes through activating JAK2/STAT3 signaling pathway, and inhibiting JAK2/STAT3 signaling with specific inhibitors could reverse SLC6A14-mediated tumorigenic effects. Besides, two different animal studies verified the tumor-promoting effect of SLC6A14 in CRC. Conclusion: Our data illustrated the crucial function that SLC6A14 played in the promotion of CRC, suggesting SLC6A14/JAK2/STAT3 axis may serve as novel therapeutic targets for patients with CRC.

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“…In the context of the PI3K/Akt pathway, the down-regulation of Small Nucleolar RNA Host Gene 3 (SNHG3) was reported to promote growth and invasiveness in vitro and in vivo via activating PI3K/Akt/ Mechanistic Target of Rapamycin Kinase (mTOR) pathway (132). However, the mechanism by which such phenotype was observed has not been elucidated.…”

Section: Pi3k/akt-mediated Tumorigenic Effects Of Dysregulated Lncrnasmentioning

confidence: 99%

Non-Coding RNAs: Uncharted Mediators of Thyroid Cancer Pathogenesis

Tabatabaeian¹,

Yang²,

Tay³

2020

Preprint

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Thyroid cancer is the most prevalent malignancy of the endocrine system and the ninth most common cancer globally. Despite the advances in the management of thyroid cancer, there are critical issues with the diagnosis and treatment of thyroid cancer that result in the poor overall survival of undifferentiated and metastatic thyroid cancer patients. Recent studies have revealed the role of different non-coding RNAs (ncRNAs), such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) that are dysregulated during thyroid cancer development or the acquisition of resistance to therapeutics, and may play key roles in treatment failure and poor prognosis of the thyroid cancer patients. Here, we systematically review the emerging roles and molecular mechanisms of ncRNAs that regulate thyroid tumorigenesis and drug response. We then propose the potential clinical implications of ncRNAs as novel diagnostic and prognostic biomarkers for thyroid cancer.

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lncRNA SNHG3 acts as a novel Tumor Suppressor and regulates Tumor Proliferation and Metastasis via AKT/mTOR/ERK pathway in Papillary Thyroid Carcinoma

Cited by 32 publications

References 31 publications

LncRNA SNHG3, a potential oncogene in human cancers

LncRNA SNHG3, a potential oncogene in human cancers

Aberrant SLC6A14 Expression Promotes Proliferation and Metastasis of Colorectal Cancer Via Enhancing the JAK2/STAT3 Pathway

Non-Coding RNAs: Uncharted Mediators of Thyroid Cancer Pathogenesis

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