CD74-ROS1 G2032R mutation transcriptionally up-regulates Twist1 in non-small cell lung cancer cells leading to increased migration, invasion, and resistance to crizotinib.

@article{Gou2018CD74ROS1GM,
  title={CD74-ROS1 G2032R mutation transcriptionally up-regulates Twist1 in non-small cell lung cancer cells leading to increased migration, invasion, and resistance to crizotinib.},
  author={Wenfeng Gou and Xuejiao Zhou and Zi Liu and Lijing Wang and Jiwei Shen and Xiaobo Xu and Zengqiang Li and Xin Zhai and Daiying Zuo and Yingliang Wu},
  journal={Cancer letters},
  year={2018},
  volume={422},
  pages={
          19-28
        }
}
The c-ros oncogene 1 (ROS1) is a receptor tyrosine kinase, which has been identified as an oncogene driver of non-small-cell lung cancer (NSCLC). Although crizotinib has a prominent effect on ROS1, resistance is inevitable. Development of the acquired ROS1 G2032R mutation has been reported as a resistant mechanism to ROS1 inhibitors in ROS1-rearranged (ROS1+) NSCLC patients. To explore the mechanism of drug resistance, we constructed the crizotinib resistance cell line, A549-CD74-ROS1 G2032R… 
MAY, a novel tubulin inhibitor, induces cell apoptosis in A549 and A549/Taxol cells and inhibits epithelial-mesenchymal transition in A549/Taxol cells.
TLDR
The results suggest that MAY induces apoptosis in A549 and A549/ taxol-resistant A549 cells and inhibits EMT in a549/Taxol cells, and could provide a promising method for the treatment of NSCLC.
Resistance mechanisms and potent-targeted therapies of ROS1-positive lung cancer
TLDR
The underlying mechanisms through which ROS1 tumor cells acquire resistance to crizotinib are discussed, and various new potent drugs which can overcome this resistance and serve as viable alternatives are summarized.
Synaptotagmin 7 in twist-related protein 1-mediated epithelial – Mesenchymal transition of non-small cell lung cancer
TLDR
Functional experiments indicated that SYT7 promoted proliferation, invasion, and metastasis and inhibited cell apoptosis of NSCLC cells in vitro and in vivo experiments showed that shSYT7 inhibited the xenograft tumor growth of NS CLC cells.
EPHA5 mutation impairs natural killer cell-mediated cytotoxicity against non-small lung cancer cells and promotes cancer cell migration and invasion.
TLDR
Evaluating the role of the EPHA5 mutation in the migration and invasion of non-small cell lung cancer cells and in modulating the killing effect of natural killer cells to NSCLC cells found it to impairs the NK cell-mediated cytotoxicity against NSCLCs.
ROS1-dependent cancers — biology, diagnostics and therapeutics
TLDR
The non-malignant and malignant biology of ROS1, the diagnostic challenges that ROS1 fusions present and the strategies to target ROS1 fusion proteins in both treatment-naive and acquired-resistance settings are discussed.
Deepening the Knowledge of ROS1 Rearrangements in Non-Small Cell Lung Cancer: Diagnosis, Treatment, Resistance and Concomitant Alterations
TLDR
This review will focus on ROS1 rearrangements, dealing with diagnostic aspects, new therapeutic options, resistance issues and the coexistence of ROS1 translocations with other molecular alterations.
HMGA2 regulates circular RNA ASPH to promote tumor growth in lung adenocarcinoma
TLDR
The findings reveal the oncogenic functions of the HMGA2-circASPH-HMGA2 axis and may be useful in developing circRNA-based therapeutic strategies for lung adenocarcinoma.
Esomeprazole overcomes paclitaxel‐resistance and enhances anticancer effects of paclitaxel by inducing autophagy in A549/Taxol cells
TLDR
It is found that A549/Taxol cells displayed a high level of resistance to paclitaxel with the resistance index up to 231, and esomeprazole is a promising chemosensitizer against pac litaxel‐resistant NSCLC by inducing autophagy.
Fibrillin 2 gene knockdown inhibits invasion and migration of lung cancer cells.
TLDR
The knockdown of the expression of FBN2 significantly inhibits the proliferation, invasion and migration abilities of lung cancer cells, and the underlying mechanism is investigated.
High glucose induces epithelial-mesenchymal transition and results in the migration and invasion of colorectal cancer cells
TLDR
It is suggested that hyperglycemia promotes EMT, proliferation, migration and invasion in CRC cells and may provide novel insights into the link between HG and CRC.
...
1
2
3
...

References

SHOWING 1-10 OF 47 REFERENCES
Molecular Changes Associated with Acquired Resistance to Crizotinib in ROS1-Rearranged Non–Small Cell Lung Cancer
TLDR
Molecular changes associated with acquired crizotinib resistance in ROS1-rearranged NSCLC are heterogeneous, including ROS1 tyrosine kinase mutations, EGFR activation, and epithelial-to-mesenchymal transition.
ZEB1 Mediates Acquired Resistance to the Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitors in Non-Small Cell Lung Cancer
TLDR
Increased ZEB1 can drive EMT-related acquired resistance to EGFR-TKIs in NSCLC and short-interfering RNA against Z EB1 reversed the EMT phenotype and restored erlotinib sensitivity in HCC4006ER cells.
The ERK–ZEB1 pathway mediates epithelial–mesenchymal transition in pemetrexed resistant lung cancer cells with suppression by vinca alkaloids
TLDR
The data indicate that pemetrexed resistance could be relieved by non-cross-resistant chemotherapeutic drugs such as vinca alkaloids and might be independent to TP53 status.
EML4-ALK induces epithelial-mesenchymal transition consistent with cancer stem cell properties in H1299 non-small cell lung cancer cells.
TLDR
It is shown that H1299 NSCLC cells stably expressing EML4-ALK acquire EMT phenotype, associated with enhanced invasive migration and increased expression of EMT-inducing transcription factors, and it is found that inhibition of ERK1/2 reversed EMT induced by EML 4-ALK in H 1299 cells.
CD74-ROS1 fusion transcripts in resected non-small cell lung carcinoma.
TLDR
The above results suggest that CD74-ROS1 fusion is involved in the carcinogenesis of a subset of NSCLCs and may contribute to the elucidation of the characteristics of ROS1 fusion-positive NSCLC in the future.
Downregulation of ROS-FIG inhibits cell proliferation, colony-formation, cell cycle progression, migration and invasion, while inducing apoptosis in intrahepatic cholangiocarcinoma cells
TLDR
The results suggest that FIG-ROS plays an oncogenic role in ICC and ROS1-6290 and FIG-363 segments may become effective therapeutic targets for ICC harboring ROS-FIG fusion protein.
The roles of BTG3 expression in gastric cancer: a potential marker for carcinogenesis and a target molecule for gene therapy
TLDR
It is found that BTG3 overexpression inhibited proliferation, induced S/G2 arrest, differentiation, autophagy, apoptosis, suppressed migration and invasion in MKN28 and MGC803 cells (p < 0.05).
Short hairpin RNA targeting Twist1 suppresses cell proliferation and improves chemosensitivity to cisplatin in HeLa human cervical cancer cells
TLDR
It is suggested that Twist1-mediated modulation of MDR1/P-gp expression plays an important role in sensitization of cervical cancer cells to cisplatin, and also indicates a novel therapeutic strategy to overcome drug resistance through inactivation of Twist1 expression in cervical cancer.
Drug resistance originating from a TGF-β/FGF-2-driven epithelial-to-mesenchymal transition and its reversion in human lung adenocarcinoma cell lines harboring an EGFR mutation
TLDR
Chemoresistance and increased PD-L1 expression caused by EMT can be successfully reverted by E MT-reverting agents, according to this study.
Effect of dasatinib on EMT-mediated-mechanism of resistance against EGFR inhibitors in lung cancer cells.
TLDR
Although dasatinib monotherapy did not reverse EMT in HCC4006ER cells, preemptive combination treatment with erlotinib and dasatisatinib prevented the emergence of acquired resistance via EMT, and led to the emerged of T790M.
...
1
2
3
4
5
...