&lt;p&gt;Carbon Nanospheres Exert Antitumor Effects Associated with Downregulation of 4E-BP1 Expression on Prostate Cancer&lt;/p&gt;

Dong, Weimin; Luo, Yunping; Zhang, Guian; Zhang, Hui; Liang, Yu‐Xiang; Zhuo, Yangjia; Liang, Yingke; Fen, Zou; Zhong, Weide

doi:10.2147/ijn.s257522

Cited by 7 publications

(4 citation statements)

References 37 publications

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“…The IHC staining assay was implemented as previously described [16]. Caspase-3 was detected with primary antibody (Abcam, ab184787) at 1 : 2400 dilution; E-cadherin was detected with primary antibody (Proteintech, 20874-1-AP) at 1 : 1800 dilution; Ki67 was detected with primary antibody (Abcam, ab15580) at 1 : 9600 dilution; MMP2 was detected with primary antibody (Proteintech, 10373-2-AP) at 1 : 100 dilution; MMP-9 was detected with primary antibody (CST, #13667) at 1 : 50 dilution; N-Cadherin was detected with primary antibody (Abcam, ab18203) at 1 : 600 dilution; PCNA was detected with primary antibody (CST, #2586) at 1 : 200 dilution; and PRKRA was detected with primary antibody (Affinity Biosciences, DF7334) at 1 : 500 dilution.…”

Section: Immunohistochemistry (Ihc)mentioning

confidence: 99%

Novel lncRNA AL033381.2 Promotes Hepatocellular Carcinoma Progression by Upregulating PRKRA Expression

Wang

Zhu

Xue

et al. 2022

Oxidative Medicine and Cellular Longevity

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Hepatocellular carcinoma (HCC) is a common malignant tumor that is characterized by aggressiveness and poor prognosis. Accumulating evidence indicates that oxidative stress plays a crucial role in carcinogenesis, whereas the potential mechanism between oxidative stress and carcinogenic effects remains elusive. In recent years, long noncoding RNAs (lncRNAs) in cancers have attracted extensive attention and have been shown to be involved in oxidative stress response and carcinogenesis. Nevertheless, the roles of lncRNA AL033381.2 in regulating the development and progression of HCC still remain unclear. The purpose of our study was to evaluate the potential effects and molecular mechanisms of AL033381.2 that may be involved in oxidative stress response in HCC. Using bioinformatics analyses based on the TCGA database, we screened and identified a novel lncRNA AL033381.2 in HCC, which may be involved in oxidative stress responses. qRT-PCR analysis revealed that AL033381.2 is upregulated in HCC tissues. Through in vitro and in vivo experiments, we found that AL033381.2 dramatically facilitates the growth and metastasis of HCC. Mechanistically, RNA pull-down experiments, mass spectrometry, PathArray™, and RIP were used to determine that AL033381.2 binds to PRKRA and may be involved in AL033381.2-mediated oncogenic functions in HCC cells. Moreover, rescue experiments demonstrated that PRKRA overexpression rescues the abilities of HCC cell proliferation, migration, and invasion that were affected by AL033381.2 knockdown. Furthermore, we produced a nanoparticle-based siRNA delivery system and tested its therapeutic effects in vivo. The results showed that the in vivo growth rate of the tumors treated with the nanoparticle/AL033381.2 siRNA complexes was dramatically lower than those treated with the nanoparticle/scramble siRNA complexes. Taken together, our results suggest that the novel lncRNA AL033381.2 may be involved in oxidative stress response by targeting oxidative stress-related genes in HCC. AL033381.2 plays vital oncogenic roles in HCC progression and may be a novel therapeutic marker for HCC diagnosis and treatment.

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Section: Immunohistochemistry (Ihc)mentioning

confidence: 99%

Novel lncRNA AL033381.2 Promotes Hepatocellular Carcinoma Progression by Upregulating PRKRA Expression

Wang

Zhu

Xue

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…Moreover, they show a good cloning ability and can break through the basement membrane from carcinoma in situ to form metastatic foci and worsen the disease through the invasion-metastasis cascade reaction. We investigated whether the combination of ZOL and SeNPs could effectively inhibit the growth of tumor cells by inhibiting the migration and invasion of tumor cells ( 45 , 46 ). According to the literature, ZOL in the concentration range of 1–100 μM is sufficient to inhibit the adhesion, migration, and bone resorption of PCa cells.…”

Section: Resultsmentioning

confidence: 99%

Functionalized Selenium Nanotherapeutics Synergizes With Zoledronic Acid to Suppress Prostate Cancer Cell Growth Through Induction of Mitochondria-Mediated Apoptosis and Cell Cycle S Phase Arrest

Zhao

2021

Front. Oncol.

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The use of established drugs in new therapeutic applications has great potential for the treatment of cancers. Nanomedicine has the advantages of efficient cellular uptake and specific cell targeting. In this study, we investigate using lentinan-functionalized selenium nanoparticles (LET-SeNPs) for the treatment of prostate cancer (PCa). We used assays to demonstrate that a combination of LET-SeNPs and zoledronic acid (ZOL) can reduce PCa cell viability in vitro. Stability and hemocompatibility assays were used to determine the safety of the combination of LET-SeNPs and ZOL. The localization of LET-SeNPs was confirmed using fluorescence microscopy. JC-1 was used to measure the mitochondrial membrane potential, while the cellular uptake, cell cycle and apoptosis were evaluated by flow cytometry. Finally, cell migration and invasion assays were used to evaluate the effects of the combination treatment on cell migration and invasion. Under optimized conditions, we found that LET-SeNPs has good stability. The combination of LET-SeNPs and ZOL can effectively inhibit metastatic PCa cells in a concentration-dependent manner, as evidenced by cytotoxicity testing, flow cytometric analysis, and mitochondria functional test. The enhanced anti-cancer effect of LET-SeNPs and ZOL may be related to the regulation of BCL2 family proteins that could result in the release of cytochrome C from the inner membranes of mitochondria into the cytosol, accompanied by induction of cell cycle arrest at the S phase, leading to irreversible DNA damage and killing of PCa cells. Collectively, the results of this study suggest that the combination of SeNPs and ZOL can successfully inhibit the growth of PCa cells.

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“…Autophagy induction by MIR34A negatively affects survival of prostate cancer cells, so that apoptosis inhibition does not block the anti-proliferative activity of MIR34A -mediatd autophagy [ 420 ]. Inorganic carbon nanomaterials have shown anti-tumor activity against prostate cancer cells via autophagy and apoptosis induction [ 421 ]. To date, a few studies have investigated nanoparticles and autophagy regulation in prostate cancer, but as autophagy is a vital process in prostate cancer, further experiments can focus how delivery of anti-tumor compounds by nanocarriers or their co-delivery with genetic tools can affect autophagy in favor of prostate cancer treatment.…”

Section: Autophagy and Prostate Cancermentioning

confidence: 99%

Targeting autophagy in prostate cancer: preclinical and clinical evidence for therapeutic response

Ashrafizadeh

Paskeh

Mirzaei

et al. 2022

J Exp Clin Cancer Res

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Prostate cancer is a leading cause of death worldwide and new estimates revealed prostate cancer as the leading cause of death in men in 2021. Therefore, new strategies are pertinent in the treatment of this malignant disease. Macroautophagy/autophagy is a “self-degradation” mechanism capable of facilitating the turnover of long-lived and toxic macromolecules and organelles. Recently, attention has been drawn towards the role of autophagy in cancer and how its modulation provides effective cancer therapy. In the present review, we provide a mechanistic discussion of autophagy in prostate cancer. Autophagy can promote/inhibit proliferation and survival of prostate cancer cells. Besides, metastasis of prostate cancer cells is affected (via induction and inhibition) by autophagy. Autophagy can affect the response of prostate cancer cells to therapy such as chemotherapy and radiotherapy, given the close association between autophagy and apoptosis. Increasing evidence has demonstrated that upstream mediators such as AMPK, non-coding RNAs, KLF5, MTOR and others regulate autophagy in prostate cancer. Anti-tumor compounds, for instance phytochemicals, dually inhibit or induce autophagy in prostate cancer therapy. For improving prostate cancer therapy, nanotherapeutics such as chitosan nanoparticles have been developed. With respect to the context-dependent role of autophagy in prostate cancer, genetic tools such as siRNA and CRISPR-Cas9 can be utilized for targeting autophagic genes. Finally, these findings can be translated into preclinical and clinical studies to improve survival and prognosis of prostate cancer patients. Graphical abstract

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<p>Carbon Nanospheres Exert Antitumor Effects Associated with Downregulation of 4E-BP1 Expression on Prostate Cancer</p>

Cited by 7 publications

References 37 publications

Novel lncRNA AL033381.2 Promotes Hepatocellular Carcinoma Progression by Upregulating PRKRA Expression

Novel lncRNA AL033381.2 Promotes Hepatocellular Carcinoma Progression by Upregulating PRKRA Expression

Functionalized Selenium Nanotherapeutics Synergizes With Zoledronic Acid to Suppress Prostate Cancer Cell Growth Through Induction of Mitochondria-Mediated Apoptosis and Cell Cycle S Phase Arrest

Targeting autophagy in prostate cancer: preclinical and clinical evidence for therapeutic response

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