High level of TXNDC9 predicts poor prognosis and contributes to the NF-κB-regulated metastatic potential in gastric cancer

Neoplasma ◽  
2021 ◽  
Author(s):  
Qun-Cao Yang ◽  
Nan Hao ◽  
Rui-Hua Li ◽  
Yuan-Yuan Duan ◽  
Yong Zhang
Oncotarget ◽  
2016 ◽  
Vol 7 (29) ◽  
pp. 46042-46055 ◽  
Author(s):  
Chao Li ◽  
Jian Chen ◽  
Yupeng Wang ◽  
Guohe Song ◽  
Chao Xiao ◽  
...  

Oncotarget ◽  
2017 ◽  
Vol 8 (27) ◽  
pp. 45031-45031 ◽  
Author(s):  
Chao Li ◽  
Jian Chen ◽  
Yupeng Wang ◽  
Guohe Song ◽  
Chao Xiao ◽  
...  

2019 ◽  
Vol 119 (8) ◽  
pp. 1108-1121 ◽  
Author(s):  
Fei Wang ◽  
Yi‐Lin Hu ◽  
Ying Feng ◽  
Yi‐Bing Guo ◽  
Yi‐Fei Liu ◽  
...  

2022 ◽  
Vol 8 (1) ◽  
Author(s):  
Longtao Huangfu ◽  
Biao Fan ◽  
Gangjian Wang ◽  
Xuejun Gan ◽  
Shanshan Tian ◽  
...  

AbstractRapid proliferation and metastasis of gastric cancer (GC) resulted in a poor prognosis in the clinic. Previous studies elucidated that long non-coding RNA (LncRNA) LINC00205 was upregulated in various tumors and participated in tumor progression. The aim of our study was to investigate the regulating role of LINC00205 in tumorigenesis and metastasis of GC. Both public datasets and our data showed that the LINC00205 was highly expressed in GC tissues and several cell lines. Notably, GC patients with high level of LINC00205 had a poor prognosis in our cohort. Mechanistically, knockdown of LINC00205 by shRNAs suppressed GC cells proliferation, migration, invasion remarkably, and induced cell cycle arrest. Based on bioinformatics prediction, we found that LINC00205 might act as a competitive endogenous RNA (ceRNA) through targeting miR-26a. The level of miR-26a had negatively correlated with LINC00205 expression and was decreased among GC cell lines, tissues, and serum samples. Our results for the first time confirmed that miR-26a was a direct target of LINC00205 and might have the potential to become a plasma marker for clinical tumor diagnosis. Indeed, LINC00205 knockdown resulted in the dramatic promotion of miR-26a expression as well as inhibition of miR-26a potential downstream targets, such as HMGA2, EZH2, and USP15. These targets were essential for cell survival and epithelial-mesenchymal transition. Importantly, LINC00205 was able to remodel the miR-26a-mediated downstream silence, which identified a new mechanism of malignant transformation of GC cells. In conclusion, this study revealed the regulating role of the LINC00205/miR-26a axis in GC progression and provided a new potential therapeutic strategy for GC treatment.


2012 ◽  
Vol 8 (8) ◽  
pp. 1168-1177 ◽  
Author(s):  
Yuan-fang Li ◽  
Dan-dan Wang ◽  
Bai-wei Zhao ◽  
Wei Wang ◽  
Chun-yu Huang ◽  
...  

Author(s):  
Ying‑Yu Ma ◽  
Yuancheng Zhang ◽  
Xiao‑Zhou Mou ◽  
Zheng‑Chuang Liu ◽  
Guo‑Qing Ru ◽  
...  

2009 ◽  
Vol 17 (1) ◽  
pp. 89-97 ◽  
Author(s):  
Yuan-Yu Wang ◽  
Zai-Yuan Ye ◽  
Zhong-Sheng Zhao ◽  
Hou-Quan Tao ◽  
Yong-Quan Chu

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Jun Liu ◽  
Jipeng Li ◽  
Ke Wang ◽  
Haiming Liu ◽  
Jianyong Sun ◽  
...  

AbstractFork-head box protein M1 (FoxM1) is a transcriptional factor which plays critical roles in cancer development and progression. However, the general regulatory mechanism of FoxM1 is still limited. STMN1 is a microtubule-binding protein which can inhibit the assembly of microtubule dimer or promote depolymerization of microtubules. It was reported as a major responsive factor of paclitaxel resistance for clinical chemotherapy of tumor patients. But the function of abnormally high level of STMN1 and its regulation mechanism in cancer cells remain unclear. In this study, we used public database and tissue microarrays to analyze the expression pattern of FoxM1 and STMN1 and found a strong positive correlation between FoxM1 and STMN1 in multiple types of cancer. Lentivirus-mediated FoxM1/STMN1-knockdown cell lines were established to study the function of FoxM1/STMN1 by performing cell viability assay, plate clone formation assay, soft agar assay in vitro and xenograft mouse model in vivo. Our results showed that FoxM1 promotes cell proliferation by upregulating STMN1. Further ChIP assay showed that FoxM1 upregulates STMN1 in a transcriptional level. Prognostic analysis showed that a high level of FoxM1 and STMN1 is related to poor prognosis in solid tumors. Moreover, a high co-expression of FoxM1 and STMN1 has a more significant correlation with poor prognosis. Our findings suggest that a general FoxM1-STMN1 axis contributes to cell proliferation and tumorigenesis in hepatocellular carcinoma, gastric cancer and colorectal cancer. The combination of FoxM1 and STMN1 can be a more precise biomarker for prognostic prediction.


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