Ras and Ras mutations in cancer

Rajasekharan, Satish Kumar; Raman, Thiagarajan

doi:10.2478/s11535-013-0158-5

Cited by 19 publications

(17 citation statements)

References 132 publications

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“…HDACiassists caspase-3, -7 and -8 activations (Rajasekharan and Raman, 2013). The study results (Table 1, 2 and Figure 3) shown that there are no mutation on H-Ras gene myeloma cell since the H-Ras expression on the cell without any addition of C. mangga Val.…”

Section: Resultsmentioning

confidence: 82%

Impact of Curcuma mangga Val. Rhizome Essential Oil to p53, Bcl-2, H-Ras and Caspase-9 expression of Myeloma Cell Line

et al. 2015

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Cancer is a disease, a public health problem, which is found in the world as well as in Indonesia. In general, some of cancer theraphies are ineffective, characterized by the resistance performance of cancer cell line, the exposed normal cell and by the side effects. Nowadays, studies to fi nd the specifi c and safely anti-cancer drugs were increased by the time. Several studies revealed that Curcuma mangga Val. Rhizome contains some secondary metabolites, essential or non-essential oil, which has cytotoxic activities to the cancer cells. Based on these anti-cancer potentials, this study has several aims to recognize anti-cancer selectivity and molecular mechanism by inducting apoptosis and inhibiting myeloma cell proliferation. To C. mangga Val. essential oil, immunocyto chemical test was performed to determine the expression of p53, caspase-9, Bcl-2, H-Ras protein while TUNEL test was performed to determine the number of apoptosis cells.The results of this study shown that anti-cancer molecular mechanism of C. mangga Val. essential oil to myeloma cell line was performed by increasing apoptosis; by increasing the expression of pro-apoptosis p53, caspase-9 protein and reducing protein which is increasing proliferation Bcl-2 and H-Ras.

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Section: Resultsmentioning

confidence: 82%

Impact of Curcuma mangga Val. Rhizome Essential Oil to p53, Bcl-2, H-Ras and Caspase-9 expression of Myeloma Cell Line

et al. 2015

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“…In the heart, 66.7% of cardiac-specific genes are in the center of one compartment (marked compartment A), while 66.1% of liver-specific genes are toward the periphery in compartment B. The locations of the Ras isoforms on the human chromosomes also differ (Pellicer 2011 ; Rajasekharan and Raman 2013 ): HRAS gene is localized to the short arm (p) of chromosome 11 at position 5, the KRAS gene is located on the p arm of chromosome 12 at position 12.1, and the NRAS gene is on chromosome 1 at position 13.2. Even though these are positions along the linear chromosome sequence organization, and to date data about their 3D locations are unavailable, the distinct locations of isoforms suggest distinct organization and expression patterns.…”

Section: Differential Ras Isoform Expressionmentioning

confidence: 99%

Ras isoform-specific expression, chromatin accessibility, and signaling

et al. 2021

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The anchorage of Ras isoforms in the membrane and their nanocluster formations have been studied extensively, including their detailed interactions, sizes, preferred membrane environments, chemistry, and geometry. However, the staggering challenge of their epigenetics and chromatin accessibility in distinct cell states and types, which we propose is a major factor determining their specific expression, still awaits unraveling. Ras isoforms are distinguished by their C-terminal hypervariable region (HVR) which acts in intracellular transport, regulation, and membrane anchorage. Here, we review some isoform-specific activities at the plasma membrane from a structural dynamic standpoint. Inspired by physics and chemistry, we recognize that understanding functional specificity requires insight into how biomolecules can organize themselves in different cellular environments. Within this framework, we suggest that isoform-specific expression may largely be controlled by the chromatin density and physical compaction, which allow (or curb) access to “chromatinized DNA.” Genes are preferentially expressed in tissues: proteins expressed in pancreatic cells may not be equally expressed in lung cells. It is the rule—not an exception, and it can be at least partly understood in terms of chromatin organization and accessibility state. Genes are expressed when they can be sufficiently exposed to the transcription machinery, and they are less so when they are persistently buried in dense chromatin. Notably, chromatin accessibility can similarly determine expression of drug resistance genes.

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“…The MAPK cascade consists of serine/threonine kinases, which convert extracellular molecules such as growth factors, hormones, tumor-promoting substances and differentiating factors, into intracellular signals for regulating cell proliferation, differentiation and survival [2]. The phosphorylated Raf1, an MAP3K, in turn activates MEK [3]. The guanine nucleotide exchange factors (GEFs) carry GTP to the RAS molecule, which becomes activated upon the changing of GDP for GTP [4].…”

mentioning

confidence: 99%

“…The cells that lack the p53 tumor suppressor gene are particularly affected by these consequences of RAS mutations, as p53 functions against the RAS oncogene [6]. It has been determined that RAS mutations are more prevalent in certain cancers but less likely associated with others, such as breast cancer [3]. Instead, most breast cancers, including ductal and lobular, are characterized by overexpression of the RAS protein [3].…”

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confidence: 99%

Role of Rat Sarcoma Virus Mutations in Cancer and Potential Target for Cancer Therapy

Murdande

2020

Future Sci. OA

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The prevalence of oncogenic rat sarcoma virus (RAS) mutations has made RAS a popular target for cancer therapies. Significant discoveries have been reported regarding cancer molecular biology following the study of RAS mutations. These discoveries are integral in shaping the era of targeted cancer therapy, with direct targeting of RAS or downstream RAS effectors, such as Grb2 and MAPK a possibility. Novel agents such as farnesyltransferase directly bind and sequester RAS. While these new agents and approaches have shown promise in preclinical and clinical studies, the complexity of RAS signaling and the potential for robust adaptive feedback continue to present substantial challenges. Therefore, the development of targeted therapies will require a detailed understanding of the properties and dependencies of specific cancers to a RAS mutation. This review provides an overview of RAS mutations and their relationship with cancer and discusses their potential as therapeutic targets.

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Ras and Ras mutations in cancer

Cited by 19 publications

References 132 publications

Impact of Curcuma mangga Val. Rhizome Essential Oil to p53, Bcl-2, H-Ras and Caspase-9 expression of Myeloma Cell Line

Impact of Curcuma mangga Val. Rhizome Essential Oil to p53, Bcl-2, H-Ras and Caspase-9 expression of Myeloma Cell Line

Ras isoform-specific expression, chromatin accessibility, and signaling

Role of Rat Sarcoma Virus Mutations in Cancer and Potential Target for Cancer Therapy

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