FNDC3B promotes epithelial-mesenchymal transition in tongue squamous cell carcinoma cells in a hypoxic microenvironment
Authors: Zhaoming Zhong
Jin Liang
Yuanyuan Xu
Change Gao
Hongxing Zhang
Chuanzheng Sun
Xiao Chen
Minjie He
Min Hong
Weiqing Liu
Journal: Oncology Reports (2018)
Discipline: CLINICAL MEDICINE
Keywords: oral tongue squamous cell carcinoma; metastasis; tumor recurrence; mechanisms; hypoxic microenvironment
Affiliations: Department of Medical Oncology, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650032, P.R. China, Department of Head and Neck Surgery, The Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650032, P.R. China, Department of Oncology, The First People's Hospital of Kunming, Kunming, Yunnan 650032, P.R. China

Abstract:  The primary reasons for the treatment failure of patients with oral tongue squamous cell carcinoma (OTSCC) are metastasis and tumor recurrence. Identifying the exact mechanisms underlying metastasis is a key point in improving patient prognosis. It has been reported that a hypoxic microenvironment plays an important role during the metastasis of malignancies. We found that the expression of fibronectin type III domain containing 3B (FNDC3B) is positively correlated with lymph node metastasis and advanced cTNM stage of OTSCC by IHC assay and correlation analysis. Furthermore, we found that knockdown of FNDC3B could suppress the migratory and invasive abilities of OTSCC cells. In addition, treating OTSCC cells with CoCl2 (a hypoxia mimetic agent) upregulated the mRNA and protein expression of FNDC3B via HIF-1Œ±. Moreover, the resultant increase in FNDC3B expression significantly induced epithelial-mesenchymal transition (EMT) in OTSCC cells. The present study elucidated the important role played by FNDC3B in OTSCC metastasis and indicates FNDC3B as a potential target for the treatment of OTSCC metastasis. However, many questions remain to be explored. 

Retracted: No

PubPeer comments:
  Images overlap , 
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 Corrigendum [27 April 2021] . ----------------------- After the publication of the article, and also the publication of a Corrigendum (see doi: 10.3892 or.2020.7744), there are further errors in the published paper that the authors wish to correct in a subsequent corrigendum. In the printed version of Fig. 5, the u201cNCu201d images were mistakenly presented in the data panels showing the results of the TCA8113 and TSCCA invasion assay experiments. Furthermore, in Fig. 4A and 6A, the u03b2-actin control bands were erroneously selected for these figures. The corrected versions of Figs. 4, 5 and 6 are shown opposite and on the next page, incorporating the correct data for Figs. 4A, 5 and 6A. These further corrections do not affect the results and conclusions of this work. The authors all agree to this Corrigendum, and are grateful to the Editor of Oncology Reports for allowing them to have the opportunity to correct these additional errors. Lastly, the authors apologize to the readership for any inconvenience these errors may have caused.   Figure 4. - After knockdown of FNDC3B, the protein and mRNA levels of FNDC3B in (A) TCA8113 and (B) TSCCA cells were significantly decreased, as measured by western blotting and real-time PCR, respectively. *P 0.05, **P 0.01, ***P 0.001 compared with the NC-transfected cells.  Figure 5. - After knockdown of FNDC3B, the invasive and migratory abilities of (A) TCA8113 and (B) TSCCA cells were significantly decreased, as assessed by Transwell assay. *P 0.05, **P 0.01, ***P 0.001 compared to the NC-transfected cells. Photomicrographs are at u00d7100 magnification.  Figure 6. - CoCl2 induces FNDC3B expression. (A) Protein expression and relative mRNA levels of FNDC3B in (B) TCA8113 and (C) TSCCA cells induced by 0.1 mM CoCl2 at the indicated times, as measured by real-time PCR and western blotting. (D) Protein expression of FNDC3B in TCA8113 cells induced by 1 mM DMOG. *P 0.05, **P 0.01, ***P 0.001 compared to the relevant control. ,