Circular RNAs in EMT-driven metastasis regulation: modulation of cancer cell plasticity, tumorigenesis and therapy resistance

Ashrafizadeh, Milad; Dai, Jingyuan; Torabian, Pedram; Nabavi, Noushin; Aref, Amir Reza; Aljabali, Alaa A. A.; Tambuwala, Murtaza; Zhu, Minglin

doi:10.1007/s00018-024-05236-w

Cited by 11 publications

(2 citation statements)

References 238 publications

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“…According to the previous discussions, the upregulation of MMP9, as a member of the matrix metalloproteinase family, can cause carcinogenesis. Without a doubt, epithelial-mesenchymal transition (EMT) is another player in cancer metastasis and therapy resistance [ 179 , 180 ]. The transformations and alterations mediated by EMT can increase the migration and metastasis, and help in the development of secondary tumors [ 181 , 182 ].…”

Section: Carcinogenic Functions Of Nf-ĸbmentioning

confidence: 99%

Versatile function of NF-ĸB in inflammation and cancer

Ma,

Hao,

Hong

et al. 2024

Exp Hematol Oncol

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Nuclear factor-kappaB (NF-ĸB) plays a crucial role in both innate and adaptive immune systems, significantly influencing various physiological processes such as cell proliferation, migration, differentiation, survival, and stemness. The function of NF-ĸB in cancer progression and response to chemotherapy has gained increasing attention. This review highlights the role of NF-ĸB in inflammation control, biological mechanisms, and therapeutic implications in cancer treatment. NF-ĸB is instrumental in altering the release of inflammatory factors such as TNF-α, IL-6, and IL-1β, which are key in the regulation of carcinogenesis. Specifically, in conditions including colitis, NF-ĸB upregulation can intensify inflammation, potentially leading to the development of colorectal cancer. Its pivotal role extends to regulating the tumor microenvironment, impacting components such as macrophages, fibroblasts, T cells, and natural killer cells. This regulation influences tumorigenesis and can dampen anti-tumor immune responses. Additionally, NF-ĸB modulates cell death mechanisms, notably by inhibiting apoptosis and ferroptosis. It also has a dual role in stimulating or suppressing autophagy in various cancers. Beyond these functions, NF-ĸB plays a role in controlling cancer stem cells, fostering angiogenesis, increasing metastatic potential through EMT induction, and reducing tumor cell sensitivity to chemotherapy and radiotherapy. Given its oncogenic capabilities, research has focused on natural products and small molecule compounds that can suppress NF-ĸB, offering promising avenues for cancer therapy.

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Section: Carcinogenic Functions Of Nf-ĸbmentioning

confidence: 99%

Versatile function of NF-ĸB in inflammation and cancer

Ma,

Hao,

Hong

et al. 2024

Exp Hematol Oncol

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“…Furthermore, EMT plays a crucial role in modulating the process of metastasis, anastasis, and stemness, making it a promising target for combinatorial drug design ( 81 ) ( 250 , 269 ). Salinomycin, mocetinostat, and metformin could effectively target EMT and they were studied significantly for their potential to overcome chemoresistance when used alongside drugs like doxorubicin, 5-FU, and gemcitabine ( 270 – 276 ).…”

Section: Integrating Anastasis With Emt and Chemoresistance And Immun...mentioning

confidence: 99%

Exploring the relationship between anastasis and mitochondrial ROS-mediated ferroptosis in metastatic chemoresistant cancers: a call for investigation

Cao,

Lu,

Beeraka

et al. 2024

Front. Immunol.

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Ferroptosis induces significant changes in mitochondrial morphology, including membrane condensation, volume reduction, cristae alteration, and outer membrane rupture, affecting mitochondrial function and cellular fate. Recent reports have described the intrinsic cellular iron metabolism and its intricate connection to ferroptosis, a significant kind of cell death characterized by iron dependence and oxidative stress regulation. Furthermore, updated molecular insights have elucidated the significance of mitochondria in ferroptosis and its implications in various cancers. In the context of cancer therapy, understanding the dual role of anastasis and ferroptosis in chemoresistance is crucial. Targeting the molecular pathways involved in anastasis may enhance the efficacy of ferroptosis inducers, providing a synergistic approach to overcome chemoresistance. Research into how DNA damage response (DDR) proteins, metabolic changes, and redox states interact during anastasis and ferroptosis can offer new insights into designing combinatorial therapeutic regimens against several cancers associated with stemness. These treatments could potentially inhibit anastasis while simultaneously inducing ferroptosis, thereby reducing the likelihood of cancer cells evading death and developing resistance to chemotherapy. The objective of this study is to explore the intricate interplay between anastasis, ferroptosis, EMT and chemoresistance, and immunotherapeutics to better understand their collective impact on cancer therapy outcomes. We searched public research databases including google scholar, PubMed, relemed, and the national library of medicine related to this topic. In this review, we discussed the interplay between the tricarboxylic acid cycle and glycolysis implicated in modulating ferroptosis, adding complexity to its regulatory mechanisms. Additionally, the regulatory role of reactive oxygen species (ROS) and the electron transport chain (ETC) in ferroptosis has garnered significant attention. Lipid metabolism, particularly involving GPX4 and System Xc- plays a significant role in both the progression of ferroptosis and cancer. There is a need to investigate the intricate interplay between anastasis, ferroptosis, and chemoresistance to better understand cancer therapy clinical outcomes. Integrating anastasis, and ferroptosis into strategies targeting chemoresistance and exploring its potential synergy with immunotherapy represent promising avenues for advancing chemoresistant cancer treatment. Understanding the intricate interplay among mitochondria, anastasis, ROS, and ferroptosis is vital in oncology, potentially revolutionizing personalized cancer treatment and drug development.

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