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KRAS increases the amount of KRAS. 62 / 75
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"The promoter of KRAS proto-oncogene contains G-quadruplex structure, which is bound and unwound by several proteins, including hnRNPA1, to enable KRAS transcription [177]."
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"Additionally, preclinical studies have shown that KRAS siRNA-engineered iExosomes decrease KRAS expression in mice, leading to suppressed cancer cell proliferation, enhanced apoptosis, inhibited metastasis, and increased overall survival without causing cytotoxic effects (Mendt et al., 2018; Kamerkar et al., 2017)."
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"23 However, the KRAS variant is associated with a BRCA1 mutation like gene expression signature, supporting the notion that there might be increased oncogenic risk in the presence of the KRAS variant and high KRAS expression and low BRCA1 expression, either through mutation or other mechanisms."
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"In previous studies, it has been shown that KRAS variants of RS61764370 interfere with the binding of Let-7 miRNA and increase the expression of KRAS XREF_BIBR."
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"Oncogenic mutations in KRAS typically occur at hotspots in the protein (e.g., codons 12, 13, and 61), increasing the steady-state levels of KRAS proteins in the GTP-bound state that are capable of driving protumorigenic signaling through downstream effector pathways, such as the mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) pathways."
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"As expected, stable transfection of Kras led to increased Kras expression and hyperactive Ras signaling (Figure S2A,B, Supporting Information), and subcutaneous C57BL/6J mice xenografts showed a significant increase in MC38K tumor growth as opposed to MC38 tumors (Figure 2A,B)."
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"reported interaction between the Myc associated zinc-finger protein MAZ and the G-quadruplex motif present in the promoter of murine KRAS resulting in activation of KRAS expression."
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"As shown in XREF_FIG, the mRNA and protein levels of KRAS were notably promoted by KRAS overexpression and were inhibited by KRAS silencing compared with the pEX and shNC groups, respectively (p < 0.01)."
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"A fraction of oncogenic Kras induced T-ALL and MPN lose wild-type Kras expression."
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"In the case of the same expressions of internal reference genes (β-actin), compared with the control groups (including Blank, LPAR, LPAR + L, LPAR + siRNANC), the expressions of K-Ras proteins were si[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Western blot analysis confirmed that KRAS transfection increased KRAS expression in silibinin treated cells."
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"KRAS siRNA effectively reduced KRAS expression, resulting in marked inhibition of p-ERK (XREF_FIG and XREF_SUPPLEMENTARY)."
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"Kras shRNA molecules reduce the expression of both WT Kras and Kras G12D and more potent constructs than shKras.54 inhibited the growth of AML 101-R (data not shown)."
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"For inhibitors of the m A-recognition protein, a compound called “7,773” has been found to bind IGF2BP1 and inhibit its interaction with KRAS RNA (139), thereby reducing the expression of KRAS protein and downstream signaling, inhibiting the cancer-promoting activity of IGF2BP1."
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"However, it has not been tested whether HIPK2 cooperates with KRAS-driven tumorigenicity in vivo, employing tissue-specific expression of oncogenic KRAS and HIPK2 knockout (KO)."
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"In contrast, while knockdown of wild-type KRAS did not significantly reduce KRAS protein expression in H358 cells, mutant specific knockdown potently and specifically reduced KRAS protein expression."
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"In humans, a change in codon composition in the gene KRAS, from rare to common codons, increases KRas protein expression and is associated with tumorigenicity."
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"KRAS, the key regulator of RAS and ERK pathway, was tightly regulated by enzyme activity of SIRT1, SIRT1 deacetylated KRAS and increased the expression of KRAS (Cheng et al., 2015a)."
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"Taking up liposome‐EV‐KRAS led to much higher KRAS expression in PKH26 lung cells (67.0%) (Figure S4b) compared with KRAS (0.01%) expressed in the lung cells of mice treated with free PKH26 dye.2.3 EV G12D-mutant KRAS complex induces lung inflammation via Fn1 mediated induction of IL-17A."
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"Western blot results indicated that KRAS-specific siRNA (si-KRAS) significantly inhibited the protein expression level of KRAS in MAC-T cells (Supplementary Figure S1)."
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"Compared with the H/R + VC group, expression of KRAS increased while expression of p-AKT decreased in the H/R + inhibitors group, but in the H/R + mimic group, expression of KRAS decreased while expre[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Aim : KRAS SNPs may increase KRAS transcription and KRAS levels."
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"KRAS siRNA inhibited KRAS expression, while scramble siRNA exerted no effect (Figure 7)."
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"Compared to the unmodified WT cells, KI of KRAS enhancer variant (chr12 :25538881 : C> T) increased the baseline KRAS expression in DMSO treated KI-Mut cells (2.7 and 2.2-fold, P < 0.001; XREF_FIG)."
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"Cre enzyme expression causes the deletion of P53 and the stop codon before the coding sequences of Kras , which activates Kras expression and drives the development of liver cancer."
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"These experiments revealed that K-Ras V12 induced a time- and concentration dependent increase in KRAS protein levels that was accompanied by an increase in DCF-fluorescence and binucleated cells."
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"By demonstrating that the KRAS enhancer variant confer gain-of-function activity to promote KRAS expression in leukemia cells, our results provide a mechanism that may explain the lack of KRAS hotspot coding mutations compared to other RAS family proteins such as NRAS."
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"This theory is supported by the discovery that tumor development is drastically decreased in mice with a codon-optimized KRAS coding sequence, which increases KRAS protein expression [ 58 ]."
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"Western blotting indicated that the expression of KRAS, YAP1, and HIF-1alpha in SNU-C1 cells was almost completely eliminated by DDX3 manipulation, KRAS silencing, or treatment with the ROS scavenger N-acetylcysteine (NAC)."
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"The authors speculated that the rare codon usage in KRAS leads to low endogenous protein levels, meaning that oncogenically activated KRAS would not be expressed highly enough to induce the senescent phenotype."
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"As shown in Figure 4A, siRNA knockdown of KRAS in cells at different concentrations decreased KRAS expression compared to non-targeting siRNA treated cells."
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"We found that all 3 T-ALL cell lines derived from oncogenic Kras mice and ~ 25% of oncogenic Kras induced T-ALL specimens lost WT Kras expression through distinct mechanisms (XREF_FIG)."
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"We also identified that a fraction of oncogenic Kras induced MPN lost WT Kras expression, at both early and late stages of MPN development (XREF_FIG)."
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"This could be caused by the increased expression of NF-κB regulator KRAS (109) as we observed elevated KRAS protein levels in total proteome after NF-κB inhibition."
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"Cytosolic delivery of Lipofectamine-complexed IpaH9.8-K27-D25-s11 resulted in a 46% reduction of GFP-KRAS levels, whereas control proteins lacking E3, binding ability, or ApP could not deplete GFP-KRAS levels."
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"Chen et al reported that as premiR-143-3p is transfected in LoVo and SW480 CRC cell, KRAS expression is significantly reduced by the inhibition of KRAS mRNA in the translational level."
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"In the four cell lines where KRAS siRNA strongly suppressed KRAS expression, we observed substantial reductions in pERK as well as in MYC protein levels (Fig. 6C), indicating a shared role of MYC in the oncogenic function of both G12 and Q61 mutants."
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"Recent studies have identified a KRAS 3 ' UTR polymorphism (rs61764370), aT-to-G nucleotide change in the 6th LCS (LCS6), that was found to increase KRAS expression by altering let-7 binding capability to the KRAS mRNA [XREF_BIBR]."
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"Indeed, there was a decent reduction in c-MYC nuclear stain in case of C-KRAS-esiRNA treatment of DLD1 tumors (XREF_FIG), meanwhile KRAS levels were also reduced by KRAS knockdown (XREF_FIG)."
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"These data indicated that upregulated H3 K27M might be a potent treatment target for diffuse midline glioma, H3 K27M-mutant exhibiting MASI of H3F3A K27M.There were previous studies where KRAS MASI elevated KRAS mRNA levels, increasing RAS activity [14, 24] and wild-type allele of KRAS has also been shown to play a pivotal role as a tumor suppressor [25]."
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"In studies of adult mouse pancreas, expression of Kras from the endogenous Kras locus does not lead to carcinoma unless a tumor suppressor such as Trp53 and/or Fbw7 is also mutated.7, 8, 9 However, with Kras expression in ducts, CP led to neoplastic changes including carcinoma in situ by 2 months."
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"Compared to the wild-type T genotype, the less-frequent variant G transcript of KRAS exerts a high stability through escaping the let-7 translational repression and causes a high level of KRAS in the cell."
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"Based on these results we hypothesized that CRNDE/hnRNPA2B1 axis promoted KRAS protein expression by translational control of KRAS mRNA.To gain further insight into its mechanism, the SUnSET assays were employed, and the results unveiled that hnRNPA2B1 strongly influenced global protein synthesis (Fig. 6J, S7B)."
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"Ambrogio et al (10) suggested that KRAS can antagonize the effect of KRAS and the loss of KRAS can accelerate cell proliferation and tumor progression through the increase of the GTPase level of KRAS ."
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"KRAS protein functions as a molecular switch cycling between ON and OFF state to affect the intracellular signaling.30 Whereas the ON switch to the active state is promoted by guanine nucleotide exchange factors (GEFs), the OFF state is regulated by GTPase-activating proteins (GAPs).33 Oncogenic alleles of KRAS lose the capability of GAP-induced GTP hydrolysis resulting in increased GTP-bound KRAS protein levels which in turn trigger the pro-growth signaling pathways."
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"XREF_BIBR, XREF_BIBR KRAS MASI may lead to elevated KRAS mRNA levels 24 and increased RAS activity in murine pancreatic adenocarcinomas and other carcinomas."
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"RAF kinases are activated by the RAS family proteins HRAS, NRAS, and KRAS, which is transcribed in two isoforms, KRAS4A and KRAS4B, arising from alternative splicing [ xref ]."
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"KRAS WT amplification in gastric cancers augments the level of KRAS WT “ON” and increases downstream oncogenic signaling (28)."
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"In the patients with metastatic CRC, a polymorphism rs1764370 in KRAS leads to loss function of let-7, increased expression of KRAS, and drug resistance of cetuximab-irinotecan chemotherapy, as well as reduced overall survival and progression-free survival 15."
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"In addition, Morpholino knocked-down zebrafish embryos of kras caused heart and craniofacial malformations, and expression of mutated kras resulted in maldevelopment of the heart."
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"LCS6 in the KRAS 3 '-UTR mRNA causes an increase in expression of KRAS in vitro and a reduction in let-7 levels in vivo (Chin et al., 2008)."
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"KRAS is upregulated in many cancers, and mutations in the KRAS gene can cause expression of aberrant KRAS proteins that promote the transformation of normal cells into cancerous cells by promoting cellular proliferation, survival, and cancer progression [88]."
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"Based on the gene knockdown results in Figure XREF_FIG, HDAC1 siRNA and K-Ras siRNA delivered by FA/GO nanoformulations could efficiently suppress the expression of HDAC1 and K-Ras, respectively."
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"A homologous promoterless K-ras cDNA targeting endogenous K-ras expression inhibits human pancreatic cancer cell growth in vitro and in vivo."
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"Liu et al. confirmed that KRAS gene SNP rs8720 CT increased mRNA and protein expression of KRAS and thus contribute to increased colorectal carcinoma (CRC) risk and reduced survival (41)."
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"Gnat3-null (Gnat3 -/-) mice were crossbred with animals harboring a Cre inducible Kras LSL-G12D/+ allele with either Ptf1a Cre/+ (KC) or tamoxifen inducible Ptf1a CreERT/+ (KC ERT) mice to drive oncogenic KRAS expression in the pancreas."
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"Kras G12D/+ mice were treated with AdCre to initiate expression of oncogenic Kras."
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"Western blotting revealed that the expression of KRAS and beta-catenin was eliminated by DDX3 or KRAS silencing, but KRAS expression was unchanged by LY294002, shDDX3 plus KRAS or shDDX3, LY294002 plus KRAS treatments in CCM2 cells."
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"Previous studies have provided preliminary evidence that the KRAS G4 can indeed be targeted with small molecules to elicit changes in KRAS expression."
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"Although we propose that KRAS downregulation is not the sole event responsible for the death of METTL3 KO epithelium, we examined whether overexpression of KRAS could rescue death of METTL3-KO enteroids to definitively determine the role of KRAS expression."
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"Inhibition of KRAS expression by selected KRAS antisense oligonucleotides has been shown to be associated with significantly reduced secretion of VEGF-A165 into the medium of colorectal cancer cell cultures [XREF_BIBR]."
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"miR-199a reduced K-RAS expression significantly, and forced expression of K-RAS restored K-RAS expression as shown in Figure 5A."
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