Yiqi Formula Enhances the Antitumor Effects of Erlotinib for Treatment of Triple‐Negative Breast Cancer Xenografts

Liao, Min; Ye, Meina; Zhou, Renhong; Sheng, Jiayu; Chen, Hongfeng

doi:10.1155/2014/628712

Cited by 14 publications

(2 citation statements)

References 33 publications

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“…Studies have demonstrated the superior effect of erlotinib (EB) on EGFR signaling pathway blocking, which results in an obvious inhibition effect of tumor cells growth, invasion and migration (Liu et al., 2017). Additionally, treating with EB also played a promoting role in accelerating cell apoptosis and disruption of angiogenesis through inhibition of the cell cycle protein kinase dependent inhibition protein p27 (p27kip1 protein) (Liao et al., 2014). In the present study, therefore, we have developed PLA-based nano-platforms and used EB as a model drug to treat TNBCs.…”

Section: Introductionmentioning

confidence: 99%

pH sensitive peptide functionalized nanoparticles for co-delivery of erlotinib and DAPT to restrict the progress of triple negative breast cancer

Liu

Lin

et al. 2019

Drug Delivery

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Although a variety of drug delivery strategies have been designed for enhancing the treatment of Triple negative breast cancer (TNBC), combating with TNBCs is still dramatically challenged by the selection of appropriate therapeutic targets and insufficient tumor accumulation or inner penetration of chemotherapeutics. To address these issues, the classical EGFR-inhibitor, erlotinib (EB), was selected as the model drug here and PLA-based nano-platform (NP-EB) was prepared for tumor site drug delivery. Given the significant role of Notch-EGFR interplay in raising severe resistance to EGFR inhibition of EB, gamma secretase inhibitor (GSI)-DAPT was further entrapped into the core of nanoparticles to inhibit the activation of Notch signaling (NP-EB/DART). For achieving the goal of tumor targeting drug delivery, we developed a new peptide CF and decorating it on the surface of EB/DART-dual loaded nanoparticles (CF-NP-EB/DART). Such CF peptide was designed by conjugating two separated peptide CREKA, tumor-homing peptide, and F3, cell penetrating peptide, to together via a pH-sensitive hydrazone bond. By this way, the tumor unspecific property of F3 was sealed and significantly reduced the site effects. However, after the nanoparticles reach the tumor site, the pH-sensitive linkage can be broken down by the unique acidic environment of tumor, and subsequently discovered the F3 peptide to penetrate into tumor cells.

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Section: Introductionmentioning

confidence: 99%

pH sensitive peptide functionalized nanoparticles for co-delivery of erlotinib and DAPT to restrict the progress of triple negative breast cancer

Liu

Lin

et al. 2019

Drug Delivery

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show abstract

“…For example, Wenshen Zhuanggu formula mitigates breast cancer bone metastasis through suppression of Jagged1/Notch and TGF-β1/Smads pathway [ 5 , 20 ]. Yiqi formula inhibited the TNBC xenograft tumor growth by reducing p-EGFR and p-AKT1 [ 21 ]. Therefore, deeply understanding the mechanisms of CHM in tumor progression may provide new perspectives for cancer treatment.…”

Section: Discussionmentioning

confidence: 99%

Ruyiping formula inhibits metastasis via the microRNA-134-SLUG axis in breast cancer

Jiang

Pei

Xie

et al. 2021

BMC Complement Med Ther

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Background Metastasis is the leading cause of death among breast cancer patients. MicroRNA-134 has been reported to have a tumor-suppressive role in breast cancer. Ruyiping (RYP), a traditional Chinese formula, has been shown with the ability to reduce breast cancer metastasis in pre-clinical studies. This present study was designed to examine whether miR-134 was involved in RYP-inhibited breast cancer metastasis. Methods The expression of SLUG, E-Cadherin, N-Cadherin and miR-134 in MDA-MB-231 and 4 T1 cells treated with RYP or vehicle control were determined by quantitative realtime-PCR and western blot. Invasiveness determined by transwell assay as well as SLUG gene expression determined by qPCR were detected in cells transfected with chemically synthesized miR-134 mimics or inhibitors. BALB/c mice were injected with 4 T1 cells orthotopically and fed with RYP through gavage. Breast tumor growth, metastasis and tumor expression of EMT markers were detected. Results Compared with the control, Ruyiping formula significantly inhibited SLUG-regulated breast cancer cells invasion. MiR-134 was induced by RYP in vitro and in vivo and was able to suppress SLUG by targeting its 3’UTR. RYP suppressed SLUG expression and cell invasion through miR-134. In 4 T1 tumor-bearing mice, RYP significantly inhibited 4 T1 tumor growth and lung metastasis, increased the levels of miR-134 and epithelial marker while decreased the levels of SLUG and mesenchymal marker. Conclusion Our data uncovered that Ruyiping formula exerts an anti-metastatic activity against breast cancer cells by regulating SLUG through miR-134. MiR-134-SLUG axis might be a promising strategy in breast cancer therapy.

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Retracted: Comparative molecular docking and molecular‐dynamic simulation of wild‐type‐ and mutant carboxylesterase with BTA‐hydrolase for enhanced binding to plastic

Lameh

Baseer

Ashiru

2021

Engineering in Life Sciences

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According to the literature review, microbial degradation of polyethylene terephthalate by PETases has been detected effective and eco-friendly. However, the number of microorganisms capable of such feats is limited with some undesirable bioprospecting results. BTA-hydrolase has been already reported capable of degrading polyethylene terephthalate. Therefore, mutation by in silico sitedirected mutagenesis means to introduce current isomer of PETase for polyethylene terephthalate degradative capability as a better approach to resolve this issue. This study aimed to use in silico site-directed mutagenesis to convert a carboxylesterase from Archaeoglobus fulgidus to BTA-hydrolase from Thermobifida fusca by replacing six amino acids in specific locations. This work was followed by molecular docking analysis with polyethylene terephthalate and polypropylene to compare their interactions. The best-docked enzyme-substrate complex was further subjected to molecular dynamics simulation to gauge the binding quality of the BTA-hydrolase, wild-type and mutant-carboxylesterase with only polyethylene terephthalate as a substrate. Results of molecular docking revealed lowest binding energy for the wild-type carboxylesterase-polypropylene complex (-7.5 kcal/mol). The root-mean-square deviation value was observed stable for BTA-hydrolase. Meanwhile, root-mean-square fluctuation was assessed with higher fluctuation for the mutated residue Lys178. Consequently, the Rg value for BTA-hydrolase-ligand complex (∼1.68 nm) was the lowest compared to the mutant and wild-type carboxylesterase. The collective data conveyed that mutations imparted a minimal change in the ability of the mutant carboxylesterase to bind to polyethylene terephthalate.

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Yiqi Formula Enhances the Antitumor Effects of Erlotinib for Treatment of Triple‐Negative Breast Cancer Xenografts

Cited by 14 publications

References 33 publications

pH sensitive peptide functionalized nanoparticles for co-delivery of erlotinib and DAPT to restrict the progress of triple negative breast cancer

pH sensitive peptide functionalized nanoparticles for co-delivery of erlotinib and DAPT to restrict the progress of triple negative breast cancer

Ruyiping formula inhibits metastasis via the microRNA-134-SLUG axis in breast cancer

Retracted: Comparative molecular docking and molecular‐dynamic simulation of wild‐type‐ and mutant carboxylesterase with BTA‐hydrolase for enhanced binding to plastic

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