AKT2 expression

Therefore, these may function as suitable biomarkers for blood cancer diagnosis and prognosis. Additional, larger-scale investigations may be required to affirm these results.

Curiously, although modestly varying among AML samples, a high AKT1 expression shows in contrast as a strong predictor of a better patient outcome. These data suggest that AKT3 and AKT1 expressions have strong, yet opposite, prognostic values.

Western blot analyses revealed pronounced reduction of E-cadherin and NCAM in the Akt3-kd cells, whereas Akt1 and Akt2 depletion upregulated E-cadherin, especially in H23 lung carcinoma cells. In summary, we identified oncogenic K-Ras4B as a key regulator of PI3-Kα-Akt signaling and Akt3 as a crucial regulator of K-Ras4B-induced modulation of E-cadherin and NCAM expression and localization.

It illustrated that MB/AKT2 had the highest gene transfection efficiency in the studied microbubbles mediated by the ultrasound, leading to the AKT2 protein expression downregulation and the strongest tumor killing effect in vitro and in vivo. In summary, a novel and biocompatible gene delivery platform via MB with both the endogenous and external targeting effects for breast cancer theranostics was developed.

Blockage of active SREBP1 and ablation of SCD1 reduced steatosis, inflammation, and tumor burden in DEN-treated Akt2 mice. Therefore, AKT2 activation is crucial for development of steatosis-associated HCC which can be treated with blockage of AKT2-SREBP1-SCD1 signaling cascade.

The optical absorption spectra analysis of the rat blood indicates the damage level induced by the MRHM group, being in concordance with the carried out biological conventional studies results, indicating an increase in the activity of hepatic enzymes, oxidative stress, Bax/Bcl2 ratio, cdk2, and AKT2 expression results, with a reduction in p53 expression. Also, PAS results suggest that phycocyanin decreases induced damage, due to the prevention of the Bax, AKT2, and p53 altered expression and the tumor progression in a HCC rat model.

Generally, targeting the circ_NRIP1/miR-515-5p/AKT2 axis and aberrant activation of the PI3K/AKT/mTOR pathway may hold promising therapeutic strategies for BTC. Our research contributes to a better understanding of the underlying biological basis of BTC and paves the way for the development of innovative treatment approaches.

Therefore, they may function as biomarkers for the diagnosis and prognosis of blood cancer. Additional, larger-scale investigations may be required to affirm our results.

Moreover, ginsenoside Rg3 treatment partially reversed AKT2 overexpression-mediated reduction in cell proliferation, migration, invasion, and tube formation. In conclusion, the above findings suggested that ginsenoside Rg3 inhibits CC progression via regulation of AKT2 expression, which might provide a potential therapeutic target for tumor therapy.

Our study suggested that CAPE can simultaneously suppress the EGFR and Akt signaling in PCa cells and is a potential therapeutic agent for advanced PCa.

Cell growth was evaluated with hemacytometer count. Pharmacological inhibition of PI3K using LY294002 resulted in decreased phosphorylation levels of AKT (Ser473 and Thr308) and β-catenin (Ser552), suggesting crosstalk between the PI3K/AKT and β-catenin pathways... Pten loss alone or accompanied with Akt2 deletion resulted in enhanced activation of β-catenin signaling and cell proliferation. These changes correlated with increased expression of AKT1 and total phosphorylated AKT in the Pten;Akt2 DM group. These findings suggest the need to further evaluate the role of AKT isoforms in the PI3K/AKT/β-catenin signaling axis and a promise for evaluation of isoform-specific inhibitors targeted at AKT to block tumor growth.

The combined usage of AKT2, CD44v6, and MT1-MMP revealed no significant change compared to CD44v6 alone. Due to the cost and practicality, we propose using CD44v6 as a predictor biomarker of ALNM in IBC-NST.

Studies demonstrated the varied expression of AKT1/2/3 in TN breast cancers primary and metastatic patient samples across ethnicities. It also demonstrated that expression of ABCG2/Snail was found enhanced during silencing AKT1 expression, while overexpression of AKT1 negatively regulates the expression of ABCG2/Snail, thus rendering cells sensitive to cisplatin mediated death. Studies suggest that the analysis of the expression of AKT isoforms can be predictive marker for the treatment choice of cisplatin and can offer useful information for its personalized use in patients.

AKT2 overexpression or miR-506-3p inhibition restored the suppression of growth and invasiveness of CRC cancer cells caused by circPTK2 silencing. The circPTK2/miR-506-3p/AKT2 axis plays a novel and essential role in promoting CRC progression, providing potential targets for CRC therapeutic modality.

Chidamide (CHI), a novel HDACi, is reported to be effective in hematological malignancies. Conclusions The combination of CHI with FLU has a synergistic anti-leukemia effect on cell proliferation arrest and apoptosis in Ph+ALL cells by targeting PI3K/AKT signaling through the p53/c-MYC axis. Our data provide experimental evidence for a new potential combination of CHI with FLU in the therapy of Ph+ALL, and the in vivo preclinical studies will further highlight the future clinical trial of the combination in clinic therapy of ALL.

A ChIP assay demonstrated JIB-04-induced reduction in H3K27me3 at the AKT2 promoter and the enrichment of KDM6B within this promoter. Overall, our results strongly suggest that the inhibitory effect of JIB-04 on HCC malignancy and the maintenance of LCSCs is mediated via targeting the KDM6B-AKT2 pathway, indicating the therapeutic potential of JIB-04.

Our results, together with the literature data, indicate that miR-126-3p exerts suppressor activity by specifically targeting components of the PIK3/AKT signaling cascade. Therefore, management of platelet-derived MV production and selective delivery of miR-126-3p to tumor cells may represent a useful tool in multimodal therapeutic approaches in BC patients.

We further tested dual therapeutic approaches by combining BX-795 with either doxorubicin or crizotinib and found synergistic and significant inhibition of NB growth, in contrast to either drug alone. Overall, our data demonstrate that BX-795 inhibits AKT pathway to inhibit NB growth, and combining BX-795 with current therapies is an effective and clinically tractable therapeutic approach for NB.

The tumor-inhibiting properties of KLF5 knockdown were substantiated in vivo. Together, our study uncovered the oncogenic role of KLF5-dependent lncRNA DANCR transcription in GC in vivo and in vitro, which implicates the miR-194/AKT2 axis in tumor growth regulation, and it may be a potential therapeutic target for human GC.

Our findings demonstrated that actein could be a strong anti-OSCC candidate. Further evaluations of its safety and effectiveness are necessary before it can be considered for clinical use.

AKT2 expression has potential as a predictor of LNM in IBC-NST. The H-score cutoff for AKT2 expression can be used as a classification guide in future studies.

Our results demonstrated that MBiRGD/CCR2 had a significantly higher gene transfection efficiency than MBiRGD, MBCCR2, or MBcontrol under ultrasound irradiation, resulting in much lower AKT2 protein expression and stronger tumor growth inhibition effects in vivo and in vitro. In conclusion, our study demonstrated a novel gene delivery system via MBiRGD/CCR2 for ultrasound molecular-imaging-guided gene therapy of breast cancer.

miR-193a-3p directly targets ALKBH5 to inhibit the growth and promote the apoptosis of glioma cells by suppressing the AKT2 pathway both in vitro and in vivo, and the physical interaction between ALKBH5 and AKT2 is essential for suppressing cell apoptosis by upregulating miR-193a-3p in glioma cells. Our study revealed that the antitumor effects of miR-193a-3p on glioma cells is due to ALKBH5 mediation of the AKT2-induced intrinsic apoptosis signaling pathway.

Importantly, transient pharmacologic inhibition of Akt activity with MK-2206 or AZD5363 inhibitors did not prevent colonization of lung tissue by TNBC cells. Taken together, these findings demonstrate that transient decrease in AMPK isoforms expression alone or in combination with Akt1 in circulating tumor cells does not synergistically reduce TNBC metastatic lung colonization. Our results also provide evidence that Akt1 and Akt2 expression serve as a bottleneck that can challenge colonization of lungs by TNBC cells.

Further rescue experiments revealed that downregulation of miR-148a-3p and overexpression of AKT2 obviously diminished the effects of HOTTIP downregulation in ovarian cancer cells. Thus, our study elucidated a novel pyroptosis-related mechanism by which HOTTIP participated in ovarian cancer progression, which might provide a theoretical reference for clinical treatment.

We conclude that MMRd endometrial organoids exhibit attenuated P4 response compared to WT. These findings suggest MMRd-related P4-resistance may occur as a precursor to EC development. Further research into the mechanisms underlying MMRd-related P4-resistance, including UPR, are needed to identify targets that can be used in prevention or early interception in MMRd-related EC development.

The upregulated AKT2 might be a result of dysregulated interaction balance between the expressions of miR-377-3p and SNHG1. Based on such discoveries, the intervention of SNHG1/miR-377-3p/AKT2 axis could be further explored in the treatment of PCa.

Moreover, in PDAC tissues, we revealed that high nuclear levels of Vav1 correlate with low Akt2 expression. Although we cannot demonstrate the mechanisms involved, our results provide new insights into the role of Vav1 in PDAC and, as targeting specific members of the Akt family is a promising therapeutic chance in solid tumors, they suggest that Vav1, by down-modulating Akt2, has potential as a molecular target in PDAC.

Our results suggest that miR-124 overexpression can negatively regulate AKT2 and thus inhibit the progression of LUAD. Therefore, the miR-124/AKT2 axis may serve as a potential target for novel therapies for LUAD.

In conclusion, blue LED irradiation suppressed pancreatic cancer cell and tumor growth by regulating AKT/mTOR signaling. Our findings indicated that blue LEDs could be used as a nonpharmacological treatment for pancreatic cancer.

AKT2 was the target gene of miR-342-3p, and miR-342-3p expression was decreased while AKT2 expression was increased in glioma tissues. High expression of miR-342-3p inhibited cell viability, invasion and migration, and reduced AKT2 expression, whereas low expression of miR-342-3p did the opposite effect. Upregulating SNHG7 might promote glioma cells viability, migration and invasion with the regulation of decreasing miR-342-3p level and increasing AKT2 level.

GBM patient stem cells and a primary in vivo culture system with high Akt2 levels also showed TTF-induced inhibition. Taken together, our results identified autophagy as a critical cell death pathway triggered by TTFs in GBM and indicate that TTF is a potential treatment option for GBM.

Rescue experiments showed that AKT2 over-expression reversed the suppression effect of siHSDL2 on cell proliferation (P<0.001), invasion (P<0.001) and migration (P<0.001) significantly. HSDL2 functions as an oncogene to promote the growth and metastasis of lung adenocarcinoma via promoting the expression of AKT2.