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MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non-Small Cell Lung Cancer

ABSTRACT: MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non-Small Cell Lung Cancer

PROVIDER: PRJNA1256417 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33339214.fastq.gz	Fastqsanger.gz
	SRR33339215.fastq.gz	Fastqsanger.gz
	SRR33339216.fastq.gz	Fastqsanger.gz
	SRR33339217.fastq.gz	Fastqsanger.gz
	SRR33339218.fastq.gz	Fastqsanger.gz

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MYLK-AS1 Enhances Glutamine Metabolism to Promote EGFR Inhibitor Resistance in Non-Small Cell Lung Cancer

Project description:Here we identified a role for the lncRNA MYLK-AS1 promoting acquired TKI resistance of lung cancer in vitro and in vivo. MYLK-AS1 bound and directly drove phase separation of interleukin enhancer binding factor 3 (ILF3), thus interacting with the 3’UTR of glutamate dehydrogenase 1 (GLUD1) to post-transcriptionally promote its mRNA stability, thus enhancing mitochondrial glutamine catabolism, promoting TKI resistance. The MYLK-AS1/ILF3/GLUD1 may be a target for overcoming TKI resistance in lung cancer.

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TUBA1C: a new potential target of LncRNA EGFR-AS1 promotes gastric cancer progression

Project description:Background: The lack of obvious symptoms of early gastric cancer (GC) as well as the absence of sensitive and specific biomarkers results in poor clinical outcomes. Tubulin is currently emerging as important regulators of the microtubule cytoskeleton and thus have a strong potential to be implicated in a number of disorders, however, its mechanism of action in gastric cancer is still unclear. Tubulin alpha-1C(TUBA1C) is a subtype of α-tubulin, high TUBA1C expression has been shown to be closely related to a poor prognosis in in various cancers,this study, for the first time, revealed the mechanism of TUBA1C promotes malignant progression of gastric cancer in vitro and in vivo. Methods: The expression of lncRNA EGFR-AS1 was detected in human GC cell lines by qRT–PCR. Mass spectrometry experiments following RNA pulldown assays found that EGFR-AS1 directly binds to TUBA1C, the CCK8, EdU, transwell, wound-healing, cell cycle assays and animal experiments were conducted to investigate the function of TUBA1C in GC. Combined with bioinformatics analyses, reveal interaction between Ki-67, E2F1, PCNA and TUBA1C by western blot. Rescue experiments furtherly demonstrated the relationship of EGFR-AS1and TUBA1C. Results: TUBA1C was proved to be a direct target of EGFR-AS1, TUBA1C promotes gastric cancer proliferation, migration and invasion by accelerating the progression of the cell cycle from the G1 phase to the S phase and activating the expression of oncogenes: Ki-67,E2F1 and PCNA. Conclusions: TUBA1C is a new potential target of LncRNA EGFR-AS1 promotes gastric cancer progression and could be a novel biomarker and therapeutic target for GC.

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