scholarly journals The Tumor Suppressor TGFBR3 Blocks Lymph Node Metastasis in Head and Neck Cancer

Cancers ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1375 ◽  
Author(s):  
Wei-Yu Fang ◽  
Yi-Zih Kuo ◽  
Jang-Yang Chang ◽  
Jenn-Ren Hsiao ◽  
Hung-Ying Kao ◽  
...  
Keyword(s):  
Head And Neck Cancer ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Oral Cancer ◽  
Tumor Suppressor ◽  
Head And Neck ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Node Metastasis ◽  
Oral Cancer Cells

The TGF-β type III receptor (TGFBR3) is an essential constituent of the TGF-β signaling. In this study, we observed a down-regulation of TGFBR3 in oral cancer, a subtype of head and neck cancer (HNC), and patients with low TGFBR3 had poor clinical outcomes. Ectopic expression of TGFBR3 decreased migration and invasion of oral cancer cells and lymph node metastasis of tumors, whereas depletion of TGFBR3 had the opposite effect. In SMAD4-positive OC-2 oral cancer cells, TGFBR3-mediated suppression requires both of its cytoplasmic interacting partners ARRB2 and GIPC1. We demonstrated that TGFBR3 induces the abundance of secreted angiogenin (ANG), a known pro-angiogenic factor, and ANG is essential and sufficient to mediate TGFBR3-dependent inhibition of migration and invasion of oral cancer cells. Notably, in SMAD4-deficient CAL-27 oral cancer cells, only GIPC1 is essential for TGFBR3-induced suppressive activity. Accordingly, HNC patients with low expressions of both TGFBR3 and GIPC1 had the poorest overall survival. In summary, we conclude that TGFBR3 is as a tumor suppressor via SMAD4-dependent and -independent manner in both tumor and stromal cells during oral carcinogenesis. Our study should facilitate the possibility of using TGFBR3-mediated tumor suppression for HNC treatment.

S-1 mediates the inhibition of lymph node metastasis in oral cancer cells

2009 ◽  
Vol 38 (5) ◽  
pp. 428
Author(s):  
H. Sato ◽  
M. Hatori ◽  
Y. Kurihara ◽  
T. Shirota ◽  
S. Shintani
Keyword(s):  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Oral Cancer ◽  
Cancer Cells ◽  
Node Metastasis ◽  
Oral Cancer Cells

scholarly journals The tRNA-Derived Fragment-3017A Promotes Metastasis by Inhibiting NELL2 in Human Gastric Cancer

2021 ◽  
Vol 10 ◽  
Author(s):  
Linhao Tong ◽  
Weixu Zhang ◽  
Bicheng Qu ◽  
Fei Zhang ◽  
Zhonghua Wu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Node Metastasis ◽  
Mechanistic Investigation

tRNA-derived fragments (tRFs) are a new classification of small non-coding RNAs (sncRNAs) derived from the specific cleavage of precursors and mature tRNAs. Accumulating recent evidence has shown that tRFs are frequently abnormal in several cancers. Nevertheless, the role of tRFs in gastric cancer and its mechanism remain unclear. In this study, we found abnormal expression of tRF-3017A (derived from tRNA-Val-TAC) in gastric cancer tissues and cell lines and confirmed its effect on promoting the invasion and migration of gastric cancer cells through functional experiments in vitro. Analysis of clinicopathologic data showed patients with higher tRF-3017A were associated with significantly higher lymph node metastasis. Mechanistic investigation implies that tRF-3017A regulates the tumor suppressor gene NELL2 through forming the RNA-induced silencing complex (RISC) with Argonaute (AGO) proteins. In this study, we found that higher tRF-3017A were associated with significantly higher lymph node metastasis in gastric cancer patients and the tRF-3017A may play a role in promoting the migration and invasion of gastric cancer cells by silencing tumor suppressor NELL2.

scholarly journals Usefulness of investigation with real-time tissue elastography to diagnose cervical lymph node metastasis in head and neck cancer

Toukeibu Gan ◽  
2010 ◽  
Vol 36 (3) ◽  
pp. 349-353
Author(s):  
Shin Rin ◽  
Tetsuro Yamashita ◽  
Michihiro Ueda ◽  
Yuichiro Asaka ◽  
Yoritoshi Nakajima ◽  
...  
Keyword(s):  
Head And Neck Cancer ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Head And Neck ◽  
Real Time ◽  
Neck Cancer ◽  
Cervical Lymph Node ◽  
Cervical Lymph Node Metastasis ◽  
Node Metastasis ◽  
Tissue Elastography

scholarly journals Upregulation of miR-205 induces CHN1 expression, which is associated with the aggressive behaviour of cervical cancer cells and correlated with lymph node metastasis

BMC Cancer ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Jianbing Liu ◽  
Yunfeng Li ◽  
Xihua Chen ◽  
Xiangbo Xu ◽  
Haoqi Zhao ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Lymph Node ◽  
High Risk ◽  
Cell Growth ◽  
Lymph Node Metastasis ◽  
Cancer Cells ◽  
Migration And Invasion ◽  
Node Metastasis ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer

Abstract Background Cervical cancer is the leading cause of cancer-related death in women worldwide. However, the mechanisms mediating the development and progression of cervical cancer are unclear. In this study, we aimed to elucidate the roles of microRNAs and a1-chimaerin (CHN1) protein in cervical cancer progression. Methods The expression of miR-205 and CHN1 protein was investigated by in situ hybridisation and immunohistochemistry. We predicted the target genes of miR-205 using software prediction and dual luciferase assays. The expression of mRNAs and proteins was tested by qRT-PCR and western blotting respectively. The ability of cell growth, migration and invasion was evaluated by CCK-8 and transwell. Cell apoptosis was analysed by flow cytometry analysis. Results We found that miR-205 and CHN1 were highly expressed in human cervical cancer tissue compared with paired normal cervical tissues. The CHN1 gene was shown to be targeted by miR-205 in HeLa cells. Interestingly, transfection with miR-205 mimic upregulated CHN1 mRNA and protein, while miR-205 inhibitor downregulated CHN1 in high-risk and human papilloma virus (HPV)-negative human cervical cancer cells in vitro,. These data suggested that miR-205 positively regulated the expression of CHN1. Furthermore, the miR-205 mimic promoted cell growth, apoptosis, migration, and invasion in high-risk and HPV-negative cervical cancer cells, while the miR-205 inhibitor blocked these biological processes. Knockdown of CHN1 obviously reduced the aggressive cellular behaviours induced by upregulation of miR-205, suggesting that miR-205 positively regulated CHN1 to mediate these cell behaviours during the development of cervical cancer. Furthermore, CHN1 was correlated with lymph node metastasis in clinical specimens. Conclusions Our findings showed that miR-205 positively regulated CHN1 to mediate cell growth, apoptosis, migration, and invasion during cervical cancer development, particularly for high-risk HPV-type cervical cancer. These findings suggested that dysregulation of miR-205 and subsequent abnormalities in CHN1 expression promoted the oncogenic potential of human cervical cancer.

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