Amplified Ferroptosis and Apoptosis Facilitated by Differentiation Therapy Efficiently Suppress the Progression of Osteosarcoma

He, Chao; Jiang, Yuhang; Guo, Yuan; Wu, Zenghui

doi:10.1002/smll.202302575

Cited by 11 publications

(3 citation statements)

References 47 publications

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“…Therefore, the additive effect of ferroptosis activation on the anti-tumoral effect of chemotherapeutic agents on cell viability can be of interest and open a new era in cancer medicine. Recent findings have evaluated the efficacy of biomimetic/biocompatible formulations and pH-responsive liposomal nanoreactors for inducing ferroptosis in cancer models [ 107 , 108 ].…”

Section: Ferroptosis In Cancermentioning

confidence: 99%

Competing endogenous RNA networks and ferroptosis in cancer: novel therapeutic targets

Nejadi Orang,

Abdoli Shadbad

2024

Cell Death Dis

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As a newly identified regulated cell death, ferroptosis is a metabolically driven process that relies on iron and is associated with polyunsaturated fatty acyl peroxidation, elevated levels of reactive oxygen species (ROS), and mitochondrial damage. This distinct regulated cell death is dysregulated in various cancers; activating ferroptosis in malignant cells increases cancer immunotherapy and chemoradiotherapy responses across different malignancies. Over the last decade, accumulating research has provided evidence of cross-talk between non-coding RNAs (ncRNAs) and competing endogenous RNA (ceRNA) networks and highlighted their significance in developing and progressing malignancies. Aside from pharmaceutical agents to regulate ferroptosis, recent studies have shed light on the potential of restoring dysregulated ferroptosis-related ceRNA networks in cancer treatment. The present study provides a comprehensive and up-to-date review of the ferroptosis significance, ferroptosis pathways, the role of ferroptosis in cancer immunotherapy and chemoradiotherapy, ceRNA biogenesis, and ferroptosis-regulating ceRNA networks in different cancers. The provided insights can offer the authorship with state-of-the-art findings and future perspectives regarding the ferroptosis and ferroptosis-related ceRNA networks and their implication in the treatment and determining the prognosis of affected patients.

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Section: Ferroptosis In Cancermentioning

confidence: 99%

Competing endogenous RNA networks and ferroptosis in cancer: novel therapeutic targets

Nejadi Orang,

Abdoli Shadbad

2024

Cell Death Dis

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“…Zhao et al 136 The apoptotic anticancer mechanism involves the activation of cytochrome c, which initiates mitochondrial apoptosis, while ferroptosis is initiated by NCOA4. 122 He et al 138…”

Section: Enhancing Sensitivity To Os Chemotherapy Through Ferroptosismentioning

confidence: 99%

Ferroptosis defense mechanisms: The future and hope for treating osteosarcoma

Ma,

Cong,

Shen

et al. 2024

Cell Biochemistry & Function

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Currently, challenges such as chemotherapy resistance, resulting from preoperative and postoperative chemotherapy, postoperative recurrence, and poor bone regeneration quality, are becoming increasingly prominent in osteosarcoma (OS) treatment. There is an urgent need to find more effective ways to address these issues. Ferroptosis is a novel form of iron‐dependent programmed cell death, distinct from other forms of cell death. In this paper, we summarize how, through the three major defense systems of ferroptosis, not only can substances from traditional Chinese medicine, antitumor drugs, and nano‐drug carriers induce ferroptosis in OS cells, but they can also be combined with immunotherapy, differentiation therapy, and other treatment modalities to significantly enhance chemotherapy sensitivity and inhibit tumor growth. Thus, ferroptosis holds great potential in treating OS, offering more choices and possibilities for future clinical interventions.

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“…Inducing ferroptosis was thought to enhance the effects of 'traditional' anti-cancer treatments that trigger other cell death pathways, mostly apoptosis. Multiple studies had shown that simultaneous targeting of apoptosis and ferroptosis can effectively bypassing chemoresistance, which was an effective strategy to inhibit OS cells [18][19][20][21]. Oridonin was reported to exhibit the anti-tumor activity via inducing ferroptosis in gastric cancer and esophageal cancer [22,23].…”

Section: Introductionmentioning

confidence: 99%

Oridonin-induced ferroptosis and apoptosis: a dual approach to suppress the growth of osteosarcoma cell

Zhang,

Hao,

Yang

et al. 2023

Preprint

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Background Osteosarcoma (OS) is one of the most common aggressive bone malignancy tumors in adolescents. With no significant advances in the treatment of OS in recent ten years, discovering new and effective anti-OS drugs became our top priority. Oridonin has been proved to mediate anti-tumor impact on OS cells, although it’s mechanism of action has not been fully understood.Methods Here, we investigated the inhibitory effect of oridonin on OS cells and its underlying mechanisms. In 143B and U2OS cells, oridonin’s pro-apoptosis and pro-ferroptosis effects on cell death, cell proliferation, cell migration, iron accumulation, mitochondrial membrane potential and lipid peroxidation production were observed. Western blot (WB) and real-time reverse transcriptase-polymerase chain reaction (RT-qPCR) were used to detect the expression levels of apoptosis and ferroptosis-relative proteins and genes. Iron assay Kit was used to evaluate the relative Fe2+ content. The mitochondrial membrane potential detection kit and ROS assay kit were used to evaluate the levels of mitochondrial membrane potential and lipid peroxidation production. The changes of oridonin’s inhibitory on malignant phenotype of OS cells were examined after treating OS cells with the ferroptosis inhibitor ferrostatin-1 (Fer-1).Results Oridonin potently inhibited OS cells viability and metastasis. Simultaneously, oridonin suppressed the expressions of BAX, cl-caspase3, SLC7A11, GPX4 and FTH1 proteins and mRNA, while promoting the expressions of Bcl-2 and ACSL4 in 143 and U2OS cells. Furthermore, we found that oridonin also boosted the accumulation of reactive oxygen species (ROS), encouraged the buildup of Fe2+, and decreased the mitochondrial membrane potential in OS cells, but this effect can be reversed by Fer-1.Conclusion Oridonin can trigger apoptosis and ferroptosis collaboratively in OS cells, making it a promising and effective agent for OS therapy.

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Amplified Ferroptosis and Apoptosis Facilitated by Differentiation Therapy Efficiently Suppress the Progression of Osteosarcoma

Cited by 11 publications

References 47 publications

Competing endogenous RNA networks and ferroptosis in cancer: novel therapeutic targets

Competing endogenous RNA networks and ferroptosis in cancer: novel therapeutic targets

Ferroptosis defense mechanisms: The future and hope for treating osteosarcoma

Oridonin-induced ferroptosis and apoptosis: a dual approach to suppress the growth of osteosarcoma cell

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