Pristimerin induces apoptosis and tumor inhibition of oral squamous cell carcinoma through activating ROS-dependent ER stress/Noxa pathway

Zhao, Qun; Cheng, Xinran; Yu, Wei; Bi, Yunbo; Guo, Jian; Ma, Qingzhao; Gong, Yingxia; He, Li; Lei, Yu

doi:10.1016/j.phymed.2021.153723

Cited by 13 publications

(3 citation statements)

References 27 publications

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“…This result is markedly outshining previous studies. For example, Zhao et al (2021) reported the cell viability of CAL27 cells exposed to high-concentration pristimerin for 24 h was 40%, and Zhou et al (2023) reported the cell viability of HN6 cells was 53% after highconcentration safflower polysaccharide treatment for 24 h.…”

Section: Discussionmentioning

confidence: 99%

An Acid-Responsive Iron-Based Nanocomposite for OSCC Treatment

Zhao,

Leng,

Wang

et al. 2024

J Dent Res

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Oral squamous cell carcinoma (OSCC) is the most common type of oral cancer, characterized by invasiveness, local lymph node metastasis, and poor prognosis. Traditional treatment and medications have limitations, making the specific inhibition of OSCC growth, invasion, and metastasis a challenge. The tumor microenvironment exhibits mildly acidity and high concentrations of H2O2, and its exploitation for cancer treatment has been widely researched across various cancers, but research in the oral cancer field is relatively limited. In this study, by loading ultra-small Prussian blue nanoparticles (USPBNPs) into mesoporous calcium–silicate nanoparticles (MCSNs), we developed an acid-responsive iron-based nanocomposite, USPBNPs@MCSNs (UPM), for the OSCC treatment. UPM demonstrated excellent dual enzyme activities, generating toxic ·OH in a mildly acidic environment, effectively killing OSCC cells and producing O2 in a neutral environment to alleviate tissue hypoxia. The results showed that UPM could effectively inhibit the proliferation, migration, and invasion of OSCC cells, as well as the growth of mice solid tumors, without obvious systemic toxicity. The mechanisms may involve UPM inducing ferroptosis of OSCC cells by downregulating the xCT/GPX4/glutathione (GSH) axis, characterized by intracellular iron accumulation, reactive oxygen species accumulation, GSH depletion, lipid peroxidation, and abnormal changes in mitochondrial morphology. Therefore, this study provides empirical support for ferroptosis as an emerging therapeutic target for OSCC and offers a valuable insight for future OSCC treatment.

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Section: Discussionmentioning

confidence: 99%

An Acid-Responsive Iron-Based Nanocomposite for OSCC Treatment

Zhao,

Leng,

Wang

et al. 2024

J Dent Res

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“…Furthermore, ROS levels enhancing apoptosis in non-small cell lung cancer A549 and H1299 cells following treatment with raddeanin A were also reported to increase the phosphorylation of the STAT3 pathway [ 21 ]. Triterpenoid pristimerin from Celastraceae and Hippocrateaceae [ 58 ], as well as Musca domestica pupae [ 59 ], upregulated apoptosis via ROS-induced endoplasmic reticulum (ER) stress in CAL-27 and SCC-15 oral squamous carcinoma and human liver cancer HepG2cells, respectively. Additionally, triterpenoids from Euphorbia macrostegia impaired mitochondrial respiration, leading to increased ROS accumulation, ultimately contributing to ER stress and apoptosis in cancer cells [ 60 ].…”

Section: Discussionmentioning

confidence: 99%

Combination of ethyl acetate fraction from Calotropis gigantea stem bark and sorafenib induces apoptosis in HepG2 cells

Chaisupasakul,

Pekthong,

Wangteeraprasert

et al. 2024

PLoS ONE

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The cytotoxicity of the ethyl acetate fraction of the Calotropis gigantea (L.) Dryand. (C. gigantea) stem bark extract (CGEtOAc) has been demonstrated in many types of cancers. This study examined the improved cancer therapeutic activity of sorafenib when combined with CGEtOAc in HepG2 cells. The cell viability and cell migration assays were applied in HepG2 cells treated with varying concentrations of CGEtOAc, sorafenib, and their combination. Flow cytometry was used to determine apoptosis, which corresponded with a decline in mitochondrial membrane potential and activation of DNA fragmentation. Reactive oxygen species (ROS) levels were assessed in combination with the expression of the phosphatidylinositol-3-kinase (PI3K)/ protein kinase B (Akt)/ mammalian target of rapamycin (mTOR) pathway, which was suggested for association with ROS-induced apoptosis. Combining CGEtOAc at 400 μg/mL with sorafenib at 4 μM, which were their respective half-IC50 concentrations, significantly inhibited HepG2 viability upon 24 h of exposure in comparison with the vehicle and each single treatment. Consequently, CGEtOAc when combined with sorafenib significantly diminished HepG2 migration and induced apoptosis through a mitochondrial-correlation mechanism. ROS production was speculated to be the primary mechanism of stimulating apoptosis in HepG2 cells after exposure to a combination of CGEtOAc and sorafenib, in association with PI3K/Akt/mTOR pathway suppression. Our results present valuable knowledge to support the development of anticancer regimens derived from the CGEtOAc with the chemotherapeutic agent sorafenib, both of which were administered at half-IC50, which may minimize the toxic implications of cancer treatments while improving the therapeutic effectiveness toward future medical applications.

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“…Several natural compounds have shown the potential to up-regulate ACGs in cancer cells followed by induction of multidirectional antineoplastic effects [36][37][38][39][40]. As we know, by enlarge naturally occurring agents bear a safe physiological pro le, thus exploiting such compounds to up-regulate ACGs in cancer cells seems to be an attractive research domain.…”

Section: Discussionmentioning

confidence: 99%

Anticancer genes (NOXA, PAR-4, TRAIL) are de-regulated in breast cancer patients and can be targeted by using a ribosomal inactivating plant protein (riproximin)

et al. 2023

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Background: Anticancer genes are endogenous enemies of transformed cells and impose antineoplastic effects upon ectopic expression. Identifying the expression pro le of these genes is a prerequisite to explore their prognostic and therapeutic relevance in cancers. In parallel, natural compounds can be explored for their ability to upregulate anticancer genes in malignant cells for therapeutic purposes. In this study, we identi ed the expression levels of anticancer genes in breast cancer clinical isolates. In addition, the potential of a puri ed and sequenced plant protein (riproximin) to induce anticancer genes in breast cancer cells was evaluated.Methodology:Expression pro les of three anticancer genes (NOXA, PAR-4, TRAIL) were identi ed by immunohistochemistry in 45 breast cancer clinical isolates. Effects of riproximin exposure on expression of the anticancer genes were explored via microarray, real-time PCR and western blot methodologies. Lastly, the bioinformatic approach was adopted to highlight the molecular/functional signi cance of the anticancer genes.Results:NOXA expression was evenly de-regulated among the clinical isolates, while PAR-4 was signi cantly down-regulated in majority of the breast cancer tissues. In contrast, a higher TRAIL expression was observed in most of the clinical samples. Expression levels of the anticancer genes were following a distinct trend in accordance with the disease severity. Riproximin showed a substantial potential of inducing the anticancer genes in breast cancer cells at transcriptomic and protein levels. The bioinformatic approach revealed involvement of anticancer genes in multiple cellular functions and signaling cascades.Conclusion:Anticancer genes were de-regulated and showed discrete expression patterns in breast cancer patient samples. Riproximin effectively induced the expression of selected anticancer genes in breast cancer cells.

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Pristimerin induces apoptosis and tumor inhibition of oral squamous cell carcinoma through activating ROS-dependent ER stress/Noxa pathway

Cited by 13 publications

References 27 publications

An Acid-Responsive Iron-Based Nanocomposite for OSCC Treatment

An Acid-Responsive Iron-Based Nanocomposite for OSCC Treatment

Combination of ethyl acetate fraction from Calotropis gigantea stem bark and sorafenib induces apoptosis in HepG2 cells

Anticancer genes (NOXA, PAR-4, TRAIL) are de-regulated in breast cancer patients and can be targeted by using a ribosomal inactivating plant protein (riproximin)

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