Tamoxifen inhibits growth, migration, and invasion of human follicular and papillary thyroid cancer cells in vitro and in vivo

Papillary thyroid cancer can dedifferentiate into a much more aggressive form of thyroid cancer, namely into anaplastic thyroid cancer. Nrf2 is commonly activated in papillary thyroid cancer, whereas its role in anaplastic thyroid cancer has not been fully explored. In this study, we used two cell lines and an animal model to examine the function of Nrf2 in anaplastic thyroid cancer. The role of Nrf2 in anaplastic thyroid cancer was investigated by a series of functional studies in two anaplastic thyroid cancer cell lines, FRO and KAT-18, and further confirmed with an in vivo study. The impact of Nrf2 on the sensitivity of anaplastic thyroid cancer cells to lenvatinib was also investigated to evaluate its potential clinical implication. We found that the expression of Nrf2 was significantly higher in anaplastic thyroid cancer cell line cells than in papillary thyroid cancer cells or normal control cells. Knockdown of Nrf2 in anaplastic thyroid cancer cells inhibited their viability and clonogenicity, reduced their migration and invasion ability in vitro, and suppressed their tumorigenicity in vivo. Mechanistically, knockdown of Nrf2 decreased the expression of Notch1. Lastly, knockdown of Nrf2 increased the sensitivity of anaplastic thyroid cancer cells to lenvatinib. As knockdown of Nrf2 reduced the metastatic and invasive ability of anaplastic thyroid cancer cells by inhibiting the Notch 1 signaling pathway and increased the cancer cell sensitivity to lenvatinib, Nrf2 could be a promising therapeutic target for patients with anaplastic thyroid cancer.

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Epidermal growth factor enhances proliferation, migration, and invasion of follicular and papillary thyroid cancer in vitro and in vivo.

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jcem.79.2.8045955 ◽

1994 ◽

Vol 79 (2) ◽

pp. 401-408 ◽

Cited By ~ 1

Author(s):

T Hoelting ◽

A E Siperstein ◽

O H Clark ◽

Q Y Duh

Keyword(s):

Thyroid Cancer ◽

Growth Factor ◽

Epidermal Growth Factor ◽

Papillary Thyroid Cancer ◽

Migration And Invasion ◽

Papillary Thyroid ◽

Epidermal Growth

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NONHSAT076754 aids ultrasonography in predicting lymph node metastasis and promotes migration and invasion of papillary thyroid cancer cells

Oncotarget ◽

10.18632/oncotarget.13725 ◽

2016 ◽

Vol 8 (2) ◽

pp. 2293-2306 ◽

Cited By ~ 9

Author(s):

Shujun Xia ◽

Chuandong Wang ◽

Xiaofeng Ni ◽

Zhongxin Ni ◽

Yijie Dong ◽

...

Keyword(s):

Thyroid Cancer ◽

Lymph Node ◽

Lymph Node Metastasis ◽

Cancer Cells ◽

Papillary Thyroid Cancer ◽

Migration And Invasion ◽

Papillary Thyroid ◽

Node Metastasis ◽

Thyroid Cancer Cells

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Adiponectin and leptin exert antagonizing effects on proliferation and motility of papillary thyroid cancer cell lines

Journal of Physiology and Biochemistry ◽

10.1007/s13105-021-00789-x ◽

2021 ◽

Author(s):

Ersilia Nigro ◽

Francesca Maria Orlandella ◽

Rita Polito ◽

Raffaela Mariarosaria Mariniello ◽

Maria Ludovica Monaco ◽

...

Keyword(s):

Cell Proliferation ◽

Thyroid Cancer ◽

Cancer Cells ◽

Papillary Thyroid Cancer ◽

Cell Lines ◽

Combined Treatment ◽

Migration And Invasion ◽

Thyroid Cancer Cell ◽

Papillary Thyroid ◽

Thyroid Cancer Cells

AbstractAdiponectin (Acrp30) and leptin, adipokines produced and secreted mainly by the adipose tissue, are involved in human carcinogenesis. Thyroid carcinomas are frequent endocrine cancers, and several evidences suggest that they are correlated with obesity. In this study, we first analyzed the expression levels and prognostic values of Acrp30, leptin, and their receptors in thyroid cancer cells. Then, we investigated the role of Acrp30 and leptin in proliferation, migration, and invasion. We found that Acrp30 treatment alone inhibits cell proliferation and cell viability in a time and dose-dependent manner; leptin alone does not influence thyroid cancer cells (BCPAP and K1) proliferation, but the combined treatment reverts Acrp30-induced effects on cell proliferation. Additionally, through wound healing and Matrigel Matrix invasion assays, we unveiled that Acrp30 inhibits thyroid cancer cell motility, while leptin induces the opposite effect. Importantly, in the combined treatment, Acrp30 and leptin exert antagonizing effects on papillary thyroid cancer cells’ migration and invasion in both BCPAP and K1 cell lines. Highlights of these studies suggest that Acrp30 and leptin could represent therapeutic targets and biomarkers for the management of thyroid cancer.

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Long Noncoding RNA CCAL Promotes Papillary Thyroid Cancer Progression by Activation of NOTCH1 Pathway

Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics ◽

10.3727/096504018x15188340975709 ◽

2018 ◽

Vol 26 (9) ◽

pp. 1383-1390 ◽

Cited By ~ 5

Author(s):

Ying Ye ◽

Yanan Song ◽

Juhua Zhuang ◽

Saifei He ◽

Jing Ni ◽

...

Keyword(s):

Thyroid Cancer ◽

Papillary Thyroid Cancer ◽

Cancer Progression ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Thyroid Tumor ◽

Migration And Invasion ◽

Papillary Thyroid

Long noncoding RNA CCAL has been reported to promote tumor progression in various human cancers, including hepatocellular carcinoma, osteosarcoma, and colorectal cancer. However, the role of CCAL in papillary thyroid cancer remains largely unknown. In the present study, we found that the expression of CCAL was upregulated in papillary thyroid tumor tissues compared to adjacent normal tissues. Moreover, the expression of CCAL was positively related with papillary thyroid cancer severity and TNM stage and predicated poor prognosis. Besides, we found that knockdown of CCAL significantly inhibited papillary thyroid cancer cell proliferation, migration, and invasion in vitro and reduced tumor growth and metastasis in vivo. We found that knockdown of CCAL dramatically decreased the expression of NOTCH1 and suppressed the activation of the NOTCH1 signaling pathway. Furthermore, overexpression of NOTCH1 rescued the proliferation, migration, and invasion in papillary thyroid cancer cells. Taken together, our data indicated that CCAL promoted papillary thyroid cancer development and progression by activation of the NOTCH1 pathway, which provided a new insight on the design of therapeutic targets.

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