Dragon (RGMb) induces oxaliplatin resistance in colon cancer cells

Shi, Ying; Huang, Xiaoxiao; Chen, Guo-Bin; Wang, Ying; Zhi, Qiang; Liu, Yuansheng; Wu, Xiaoling; Wang, Lifen; Yang, Bing; Xiao, Chuanxing; Huang, Xing; Ren, Jianlin; Xia, Yin; Guleng, Bayasi

doi:10.18632/oncotarget.10338

Cited by 14 publications

(15 citation statements)

References 34 publications

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“…Although the early symptoms of CRC are difficult to detect, tumor progression and metastasis often presents with symptoms such as changes in stool habits, hematochezia and emaciation (2). Current treatment regimens for CRC include surgery, radiotherapy and chemotherapy; however, surgery is largely ineffective for patients with advanced-stage disease and the side effects of radiotherapy and chemotherapy are severe, with chemoresistance often posing a major challenge (3,4). Thus, there is an urgent need to identify novel oncogenes that may be driving CRC tumorigenesis, which may serve as effective diagnostic markers and therapeutic targets to facilitate the diagnosis of early-stage CRC and block tumor development.…”

Section: Introductionmentioning

confidence: 99%

Upregulated NTF4 in colorectal cancer promotes tumor development via regulating autophagy

et al. 2020

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Autophagy plays a key role in colorectal cancer (CRC) development and reduces the sensitivity of CRC cells to treatment. The present study reported a novel tumor-suppressive role for autophagy, which was demonstrated to be regulated through the novel oncogene neurotrophin-4 (NTF4). NTF4 was significantly overexpressed in tumor tissue compared with non-tumor mucosa, and the upregulation of NTF4 in CRC was associated with poor overall survival and advanced TNM stage. The genetic knockdown of NTF4 using short hairpin RNA in CRC cells prevented epithelial-to-mesenchymal transition and activated autophagy; this was regulated through the interaction between autophagy-associated gene 5 (Atg5) and the mitogen-activated protein kinase pathway. In addition, the knockdown of NTF4 inhibited cell invasion, migration, proliferation and colony formation, and promoted cell cycle arrest. Treatment of the cells with the autophagy inhibitor chloroquine (CQ) rescued these functions and promoted cell invasion, migration, proliferation and colony formation. Finally, the knockdown of NTF4 inhibited the growth of subcutaneous xenografts in Balb/c-nu mice. In conclusion, these findings suggested that NTF4 may be a diagnostic marker associated with the overall survival and progression of patients with CRC. NTF4 was found to promote tumorigenesis and CRC development through autophagy regulation.

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Section: Introductionmentioning

confidence: 99%

Upregulated NTF4 in colorectal cancer promotes tumor development via regulating autophagy

et al. 2020

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“…Despite recent advances in modern medical technology CRC remains a disease with high mortality due to local relapse, distant metastases and resistance to chemotherapy [2, 3]. CRC is associated with multiple factors and a complex mechanism of interrelated processes, and presently, it is mainly treated by surgical removal of the focal lesions, chemotherapy in combination with radiotherapy, and other palliative methods.…”

Section: Introductionmentioning

confidence: 99%

Osteopontin Promotes Cell Migration and Invasion, and Inhibits Apoptosis and Autophagy in Colorectal Cancer by activating the p38 MAPK Signaling Pathway

Huang

Quan

Chen

et al. 2017

Cell Physiol Biochem

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Background: Osteopontin (OPN) is highly expressed in colorectal cancer (CRC) and is associated with disease progression in vivo. High levels of OPN have been demonstrated to predict low survival rates in CRC. Autophagy is a process of self-digestion, which is thought to play a significant role in carcinogenesis. However, the mechanisms of OPN's effects on CRC cell autophagy have not been elucidated. Therefore, we aimed to investigate possible mechanisms of OPN's effects on CRC autophagy. Methods: HCT116 cell proliferation, apoptosis, and migration and invasion ability were identified by cell counting k¡t-8 assay, flow cytometry, wound healing assay, and transwell chamber invasion assay, respectively. The ratios of proteins LC3-II/LC3-I, P62, and Atg7 were analyzed by Western-blot. Expressions of Beclin-1, Atg4b, Bnip3, and Vps34, both in transcriptional and translational levels, were analyzed and compared by RT-PCR and Western blot. Immunofluorescence and co-focusing experiments were used to investigate the formation of autophagosomes. Results: The results showed that OPN can promote cell proliferation, migration, and invasion, as well as inhibit cell apoptosis. It was also demonstrated that OPN could inhibit cell autophagy. Further experiments revealed that the inhibitory effect of OPN on autophagy could be reversed by blocking the p38 MAPK pathway in HCT116 cells. Conclusion: OPN is involved in HCT116 cell progression and is capable of inhibiting cell autophagy possibly by activating the p38 MAPK signaling pathway, implying that OPN could be a potential novel molecular therapeutic biomarker in patients with CRC.

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“…Based on the scientific advances in affected gene detection by different technologies including gene expression tools, CRC could be classified into different molecular subtypes ( 7 ). Though improvement of comprehensive treatment has been made, CRC is clinically resistant to conventional chemotherapy treatments ( 8 , 9 ). Consequently, there is an urgent need to develop natural anticancer compounds which have higher efficacy and lower toxicity in the treatment of CRC.…”

Section: Introductionmentioning

confidence: 99%

Sanggenon C induces apoptosis of colon cancer cells via inhibition of NO production, iNOS expression and ROS activation of the mitochondrial pathway

et al. 2017

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Sanggenon C is a well-known, major active agent of the flavonoid derivative of benzopyrone with valuable biological properties, including anticancer, anti-inflammatory, antimicrobial, antiviral, antithrombotic, and immune-modulatory activities. In this study, we investigated the molecular mechanisms by which sanggenon C mediated the induction of cell death in colorectal cancer cells (CRC). Treatment of colorectal cancer cells (LoVo, HT-29 and SW480) with sanggenon C (0, 5, 10, 20, 40 and 80 µM) resulted in inhibited proliferation of colon cancer cells. In addition, Sanggenon C (10, 20, 40 µM) induces apoptosis of HT-29 colon cancer cells as well as the increased ROS generation. Furthermore, treatment with sanggenon C increased the level of intracellular Ca2+ and ATP, while inhibited the nitric oxide production via inhibiting inducible nitric oxide synthase expression. This resulted in the activation of mitochondrial apoptosis pathway as evidenced by the decrease in Bcl-2 protein expression. Consistently, the anti-growth and pro-apoptosis effects of sanggenon C on xenograft colon tumor were further confirmed in vivo. Collectively, our results demonstrated sanggenon C induced apoptosis of colon cancer cells by increased reactive oxygen species generation and decreased nitric oxide production, which is associated with inhibition of inducible nitric oxide synthase expression and activation of mitochondrial apoptosis pathway.

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Dragon (RGMb) induces oxaliplatin resistance in colon cancer cells

Cited by 14 publications

References 34 publications

Upregulated NTF4 in colorectal cancer promotes tumor development via regulating autophagy

Upregulated NTF4 in colorectal cancer promotes tumor development via regulating autophagy

Osteopontin Promotes Cell Migration and Invasion, and Inhibits Apoptosis and Autophagy in Colorectal Cancer by activating the p38 MAPK Signaling Pathway

Sanggenon C induces apoptosis of colon cancer cells via inhibition of NO production, iNOS expression and ROS activation of the mitochondrial pathway

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