The gene is frequently mutated and abnormally activated in many cancers，and plays an important role in cancer development. Metabolic reprogramming occurs in malignant tumors，which can be one of the key targets for anti-tumor therapy. gene can regulate lipid metabolism through AKT-mTORC1 single axis or multiple pathways，such as lipid synthesis pathways and degradation pathways. Similarly，lipid metabolism can also modify and activate RAS protein and its downstream signaling pathways. This article overviews the current research progress on the interaction between lipid metabolism and ，to provide insight in therapeutic strategies of lipid metabolism for -driven tumors.
Genes, ras ; Humans ; Lipid Metabolism/genetics* ; Neoplasms/genetics* ; Signal Transduction ; ras Proteins/metabolism*

Antineoplastic Agents ; therapeutic use ; Colorectal Neoplasms ; drug therapy ; genetics ; metabolism ; Genes, ras ; genetics ; Humans ; Lung Neoplasms ; drug therapy ; genetics ; metabolism ; Molecular Targeted Therapy ; methods ; Mutation ; Neoplasms ; drug therapy ; genetics ; metabolism ; Pancreatic Neoplasms ; drug therapy ; genetics ; metabolism ; Proto-Oncogene Proteins ; genetics ; metabolism ; Proto-Oncogene Proteins p21(ras) ; Receptor, Epidermal Growth Factor ; drug effects ; metabolism ; Signal Transduction ; ras Proteins ; genetics ; metabolism

OBJECTIVETo investigate the role of the epigenetic inactivation of Ras association domain family 2 (RASSF2) in the occurrence and development of prostate cancer by detecting the methylation and protein expression of RASSF2 in the tissues of prostate cancer and prostatic hyperplasia.

METHODSWe obtained genome DNA from 30 formalin-fixed paraffin-embedded specimens of prostate cancer (experimental group) and another 30 of prostatic hyperplasia (control group). We detected the methylation of RASSF2 by methylation-specific PCR (MSP) and its protein expression by immunohistochemistry.

RESULTSThe rates of RASSF2 promoter hypermethylation and the absence of its protein expression were 66.7% (20/30) and 70.0% (21/30) respectively in the experimental group, significantly higher than 6.7% (2/30) and 3.3% (1/30) in the control group (P < 0.05). The promoter hypermethylation of RASSF2 was significantly correlated with the absence of its protein expression (P < 0.05).

CONCLUSIONThe epigenetic inactivation of RASSF2 is involved in the occurrence of prostate cancer, and is expected to be a target of molecular diagnosis and treatment of prostate cancer.

DNA Methylation ; Epigenesis, Genetic ; Genes, ras ; Humans ; Male ; Prostatic Neoplasms ; genetics ; metabolism ; Tumor Suppressor Proteins ; genetics ; metabolism

Antineoplastic Agents ; pharmacology ; Autophagy ; drug effects ; Disulfides ; pharmacology ; Gene Expression Regulation, Neoplastic ; Glycogen Synthase Kinase 3 ; genetics ; metabolism ; HCT116 Cells ; Humans ; Piperazines ; pharmacology ; Proto-Oncogene Proteins ; genetics ; metabolism ; Proto-Oncogene Proteins p21(ras) ; Signal Transduction ; ras Proteins ; genetics ; metabolism

Adenocarcinoma, Follicular ; genetics ; metabolism ; pathology ; Biomarkers, Tumor ; genetics ; Diagnosis, Differential ; Humans ; Matrix Metalloproteinase 1 ; biosynthesis ; genetics ; Telomerase ; biosynthesis ; genetics ; Thyroid Neoplasms ; genetics ; metabolism ; pathology ; ras Proteins ; biosynthesis ; genetics

OBJECTIVETo investigate the effect of microRNA143 on cell proliferation and K-ras expression in colorectal carcinoma.

METHODSNorthern blot was used to examine the expression of miR-143 in colorectal carcinoma and adjacent normal tissues. A miR-143 expression vector was constructed and transfected into a human colon adenocarcinoma cell line SW480. Cell proliferation was evaluated by MTT assay. RT-PCR and Western blot were used to examine the expression of K-ras oncogene in transfected cells.

RESULTSThe level of mature miR-143 was lower in tumors compared with adjacent normal tissues in 81% of colorectal carcinoma specimens. In transfected cells, the increased accumulation of miR-143 inhibited the cell proliferation, and resulted in approximately 40.3% decrease of K-ras protein levels, but had no effect on level of K-ras mRNA.

CONCLUSIONThe increased accumulation of miR-143 inhibits the proliferation of transfected cells, and results in down-regulation of K-ras protein in colorectal carcinoma.

Adenocarcinoma ; genetics ; metabolism ; pathology ; Cell Line, Tumor ; Cell Proliferation ; Colonic Neoplasms ; genetics ; metabolism ; pathology ; Down-Regulation ; Genes, ras ; Genetic Vectors ; Humans ; MicroRNAs ; genetics ; metabolism ; Plasmids ; RNA, Messenger ; metabolism ; Transfection ; ras Proteins ; metabolism

OBJECTIVETo elucidate the role of let-7d in regulating the biological behavior of ovarian cancer cells and their expressions of HMGA2 and ras proteins.

METHODSThe pre-let-7d sequence was synthesized and inserted into pcDNA6.2GW/EmGFPmiR and transfected into ovarian cancer IGROV1 cells to cause pre-let-7d overexpression. Real-time quantitative RT-PCR was employed to examine the expression levels of let-7d miRNA and HMGA2 mRNA, and Western blotting was performed to detect the expressions of HMGA2 and ras protein in the transfected cells. The effect of pcDNA6.2GW-let-7d transfection on IGROV1 cell proliferation was determined using MTT assay and the cell apoptosis rate was measured using flow cytometry.

RESULTSThe eukaryotic expression vector containing the target gene let-7d was successfully constructed and transfected into IGROV1 cells. The transfected cells showed a marked reduction of HMGA2 expression but a less obvious down-regulation of ras expression. Transfection with pcDNA6.2GW-let-7d to suppress the expression of HMGA2 caused alterations of the phenotype of IGROV1 cells shown by a reduced proliferative activity and increased cell apoptosis.

CONCLUSIONLet-7d plays an important role in altering the malignant cell phenotype of ovarian cancer IGROV1 cells by regulating the expression of HMGA2.

Cell Line, Tumor ; Female ; Gene Expression Regulation, Neoplastic ; HMGA2 Protein ; genetics ; metabolism ; Humans ; MicroRNAs ; genetics ; Ovarian Neoplasms ; genetics ; metabolism ; pathology ; Plasmids ; ras Proteins ; genetics ; metabolism

Female ; Genes, p53 ; immunology ; Humans ; Ovarian Neoplasms ; genetics ; pathology ; Ovary ; pathology ; Proto-Oncogene Proteins ; immunology ; metabolism ; Proto-Oncogene Proteins p21(ras) ; Proto-Oncogenes ; immunology ; Sertoli-Leydig Cell Tumor ; genetics ; pathology ; ras Proteins ; immunology ; metabolism

Humans ; Proto-Oncogene Proteins p21(ras)/genetics* ; Prognosis ; Biomarkers, Tumor/genetics* ; Mutation/genetics* ; Colorectal Neoplasms/genetics* ; Proto-Oncogene Proteins B-raf/metabolism*

Neuronal atrophy is a common pathological feature occurred in aging and neurodegenerative diseases. A variety of abnormalities including motor protein malfunction and mitochondrial dysfunction contribute to the loss of neuronal architecture; however, less is known about the intracellular signaling pathways that can protect against or delay this pathogenic process. Here, we show that the DYNC1I1 deficiency, a neuron-specific dynein intermediate chain, causes neuronal atrophy in primary hippocampal neurons. With this cellular model, we are able to find that activation of RAS-RAF-MEK signaling protects against neuronal atrophy induced by DYNC1I1 deficiency, which relies on MEK-dependent autophagy in neuron. Moreover, we further reveal that BRAF also protects against neuronal atrophy induced by mitochondrial impairment. These findings demonstrate protective roles of the RAS-RAF-MEK axis against neuronal atrophy, and imply a new therapeutic target for clinical intervention.
Animals ; Cell Line ; Cytoplasmic Dyneins ; genetics ; metabolism ; Hippocampus ; metabolism ; pathology ; MAP Kinase Kinase Kinases ; genetics ; metabolism ; MAP Kinase Signaling System ; Mice ; Mice, Knockout ; Neurodegenerative Diseases ; genetics ; metabolism ; pathology ; Proto-Oncogene Proteins B-raf ; genetics ; metabolism ; ras Proteins ; genetics ; metabolism