Correction: Resveratrol reverses Doxorubicin resistance by inhibiting epithelial-mesenchymal transition (EMT) through modulating PTEN/ Akt signaling pathway in gastric cancer

Xu, Jiahui; Liu, Deying; Niu, Huilin; Zhu, Gangjie; Xu, Yangwei; Ye, Danli; Li, Jian; Zhang, Qingling

doi:10.1186/s13046-023-02593-5

Cited by 3 publications

(3 citation statements)

References 1 publication

(1 reference statement)

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“…The fluorescence absorption value measured by a microplate reader can reflect mitochondrial function and indirectly count live cells . [143] The MTT experiment operates on a similar principle, but Formazan is produced through the reduction of exogenous MTT by succinate dehydrogenase in mitochondria. [144] DNA proliferation detection includes EdU, BrdU, and Propidium iodide strategies, among which EdU is Transwell Detecting cell migration, chemotaxis and invasion [117] Tube formation Immunohistochemical Reflecting endothelial cell function [133] most widely used in wh-eEVs.…”

Section: Biological Effects In Vitromentioning

confidence: 99%

“…The scratch assay is a measure of various cells' migration ability, emulating the in vitro healing process. [ 143 ] In this method, a “scratch,” or cell‐free zone, is created within a single layer of cells. The cells around this scratch proliferate and migrate towards the empty space, effectively filling it up.…”

Section: Design and Research Paradigms Of Engineered Evs Applied In W...mentioning

confidence: 99%

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Engineered Extracellular Vesicles in Wound Healing: Design, Paradigms, and Clinical Application

Liao,

Zhang,

Ouyang

et al. 2023

Small

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The severe quality of life and economic burden imposed by non‐healing skin wounds, infection risks, and treatment costs are affecting millions of patients worldwide. To mitigate these challenges, scientists are relentlessly seeking effective treatment measures. In recent years, extracellular vesicles (EVs) have emerged as a promising cell‐free therapy strategy, attracting extensive attention from researchers. EVs mediate intercellular communication, possessing excellent biocompatibility and stability. These features make EVs a potential tool for treating a plethora of diseases, including those related to wound repair. However, there is a growing focus on the engineering of EVs to overcome inherent limitations such as low production, relatively fixed content, and targeting capabilities of natural EVs. This engineering could improve both the effectiveness and specificity of EVs in wound repair treatments. In light of this, the present review will introduce the latest progress in the design methods and experimental paradigms of engineered EVs applied in wound repair. Furthermore, it will comprehensively analyze the current clinical research status and prospects of engineered EVs within this field.

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Section: Biological Effects In Vitromentioning

confidence: 99%

Section: Design and Research Paradigms Of Engineered Evs Applied In W...mentioning

confidence: 99%

Engineered Extracellular Vesicles in Wound Healing: Design, Paradigms, and Clinical Application

Liao,

Zhang,

Ouyang

et al. 2023

Small

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“…69 Additionally, it promotes cell invasion by regulating the E-cadherin/β-catenin complex, exerting a more critical impact on the metastatic process than the complex itself. 70 PL was shown to significantly inhibit HCC by impeding EMT. In previous studies, PL inhibited HCC tumor angiogenesis, invasion, and metastasis, and induced autophagy-apoptosis interaction.…”

mentioning

confidence: 98%

Plumbagin Regulates Snail to Inhibit Hepatocellular Carcinoma Epithelial-Mesenchymal Transition in vivo and in vitro

Du,

Yuan,

et al. 2024

JHC

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Background/Aims: Plumbagin (PL) has been shown to effe ctively inhibit autophagy, suppressing invasion and migration of hepatocellular carcinoma (HCC) cells. However, the specific mechanism remains unclear. This study aimed to investigate the effect of PL on tumor growth factor (TGF)-β-induced epithelial-mesenchymal transition (EMT) in HCC. Methods: Huh-7 cells were cultured, and in vivo models of EMT and HCC-associated lung metastasis were developed through tail vein and in situ injections of tumor cells. In vivo imaging and hematoxylin and eosin staining were used to evaluate HCC modeling and lung metastasis. After PL intervention, the expression levels of Snail, vimentin, E-cadherin, and N-cadherin in the liver were evaluated through immunohistochemistry and Western blot. An in vitro TGF-β-induced cell EMT model was used to detect Snail, vimentin, E-cadherin, and N-cadherin mRNA levels through a polymerase chain reaction. Their protein levels were detected by immunofluorescence staining and Western blot. Results:In vivo experiments demonstrated that PL significantly reduced the expression of Snail, vimentin, and N-cadherin, while increasing the expression of E-cadherin at the protein levels, effectively inhibiting HCC and lung metastasis. In vitro experiments confirmed that PL up-regulated epithelial cell markers, down-regulated mesenchymal cell markers, and inhibited EMT levels in HCC cells. Conclusion: PL inhibits Snail expression, up-regulates E-cadherin expression, and down-regulates N-cadherin and vimentin expression, preventing EMT in HCC cells and reducing lung metastasis.

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Cancer resistance via the downregulation of the tumor suppressors RKIP and PTEN expressions: therapeutic implications

Moghaddam

Vivarelli

Falzone

et al. 2023

Exploration of Targeted Anti-Tumor Therapy

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The Raf kinase inhibitor protein (RKIP) has been reported to be underexpressed in many cancers and plays a role in the regulation of tumor cells’ survival, proliferation, invasion, and metastasis, hence, a tumor suppressor. RKIP also regulates tumor cell resistance to cytotoxic drugs/cells. Likewise, the tumor suppressor, phosphatase and tensin homolog (PTEN), which inhibits the phosphatidylinositol 3 kinase (PI3K)/AKT pathway, is either mutated, underexpressed, or deleted in many cancers and shares with RKIP its anti-tumor properties and its regulation in resistance. The transcriptional and posttranscriptional regulations of RKIP and PTEN expressions and their roles in resistance were reviewed. The underlying mechanism of the interrelationship between the signaling expressions of RKIP and PTEN in cancer is not clear. Several pathways are regulated by RKIP and PTEN and the transcriptional and post-transcriptional regulations of RKIP and PTEN is significantly altered in cancers. In addition, RKIP and PTEN play a key role in the regulation of tumor cells response to chemotherapy and immunotherapy. In addition, molecular and bioinformatic data revealed crosstalk signaling networks that regulate the expressions of both RKIP and PTEN. These crosstalks involved the mitogen-activated protein kinase (MAPK)/PI3K pathways and the dysregulated nuclear factor-kappaB (NF-κB)/Snail/Yin Yang 1 (YY1)/RKIP/PTEN loop in many cancers. Furthermore, further bioinformatic analyses were performed to investigate the correlations (positive or negative) and the prognostic significance of the expressions of RKIP or PTEN in 31 different human cancers. These analyses were not uniform and only revealed that there was a positive correlation between the expression of RKIP and PTEN only in few cancers. These findings demonstrated the existence of signaling cross-talks between RKIP and PTEN and both regulate resistance. Targeting either RKIP or PTEN (alone or in combination with other therapies) may be sufficient to therapeutically inhibit tumor growth and reverse the tumor resistance to cytotoxic therapies.

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Correction: Resveratrol reverses Doxorubicin resistance by inhibiting epithelial-mesenchymal transition (EMT) through modulating PTEN/ Akt signaling pathway in gastric cancer

Cited by 3 publications

References 1 publication

Engineered Extracellular Vesicles in Wound Healing: Design, Paradigms, and Clinical Application

Engineered Extracellular Vesicles in Wound Healing: Design, Paradigms, and Clinical Application

Plumbagin Regulates Snail to Inhibit Hepatocellular Carcinoma Epithelial-Mesenchymal Transition in vivo and in vitro

Cancer resistance via the downregulation of the tumor suppressors RKIP and PTEN expressions: therapeutic implications

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