Non-coding RNAs targeting notch signaling pathway in cancer: From proliferation to cancer therapy resistance

Hashemi, Mehrdad; Hasani, Sahar; Hajimazdarany, Shima; Mirmazloomi, Seyed Reza; Makvandy, Sara; Zabihi, Abbas; Goldoost, Yeganeh; Gholinia, Nazanin; Kakavand, Amirabbas; Tavakolpournegari, Alireza; Salimimoghadam, Shokooh; Nabavi, Noushin; Zarrabi, Ali; Taheriazam, Afshin; Entezari, Maliheh; Hushmandi, Kiavash

doi:10.1016/j.ijbiomac.2022.09.203

Cited by 15 publications

(8 citation statements)

References 217 publications

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“…Proliferation, a hallmark of cancer, plays a pivotal role in tumor treatment strategies [33]. Celastrol, for example, exhibits its therapeutic potential by effectively restraining laser-induced choroidal neovascularization, primarily through the suppression of VEGF-induced proliferation [34].…”

Section: Discussionmentioning

confidence: 99%

Celastrol can inhibit the growth of SHH medulloblastoma: In vitro and in vivo studies

王,

徐,

余

et al. 2024

Preprint

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Celastrol is a naturally occurring compound with a range of pharmacological properties derived from the traditional Chinese herb Tripterygium wilfordii. To develop a new therapeutic strategy for medulloblastoma (MB), this study will investigate the inhibitory effect of celastrol on MB and its underlying signaling pathway. We evaluated the effects of celastrol on cell proliferation using the CCK-8 assay and colony formation assay. Scratch assays and transwell invasion assays were used to assess the effects of celastrol on metastasis. The flow cytometry method was used to detect apoptosis and reactive oxygen species (ROS) levels in the cells. The potential signaling pathways were detected by transcriptomics and quantitative PCR. To study the anticancer effect of celastrol on MB in vivo using a mouse xenograft model. Cell proliferation and metastasis of the SHH subgroup MB cell line can be inhibited by celastrol, and the effect of the drug on apoptosis is associated with its proliferation inhibition effect. Animal experiments showed that celastrol inhibited the growth of MB in vivo. In addition, the pro-apoptotic effect of celastrol on ONS-76 cells may be caused by ROS. Our findings indicate that celastrol inhibits the progression of MB both in vitro and in vivo, and this effect is associated with the induction of ROS in cells by celastrol in vitro studies.

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Section: Discussionmentioning

confidence: 99%

Celastrol can inhibit the growth of SHH medulloblastoma: In vitro and in vivo studies

王,

徐,

余

et al. 2024

Preprint

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“…The Wnt/β-catenin pathway is an important regulatory pathway of bone formation that plays a key role in bone homeostasis and bone repair. The mechanism of the Wnt/β-catenin pathway in bone metabolism has been continuously studied and has become a new hotspot in the pathogenesis and treatment of bone metabolic diseases [35]. When extracellular Wnt binds with the membrane receptor Frizzled, dimers are formed through a series of interactions between membrane and cytoplasmic proteins, allowing β-catenin to accumulate in the cytoplasm.…”

Section: Discussionmentioning

confidence: 99%

Bone protection mechanism of Zuogui Pill in an osteoporosis model of breast cancer rats after endocrine therapy

ao,

Chunhui,

Lei

et al. 2023

Preprint

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Background Postmenopausal breast cancer patients treated with aromatase inhibitors (AIs) have an increased risk of developing secondary osteoporosis. Zuogui Pill has been proven to have obvious preventative and therapeutic effects against osteoporosis in the clinic. However, the possible mechanism of this bone-protective mechanism of Zuogui Pill is still largely unknown.Methods An osteoporosis model of postmenopausal breast cancer was generated by gavage of letrozole in ovariectomized mice with breast cancer. Serum oestradiol (E2), bone alkaline phosphatase (BALP), and amino terminal propeptide of type Ⅰ collagen (PINP) were detected by enzyme-related immunosorbent assays (ELISAs). After death, the right femur and tibia were taken and stained with HE to observe the bone histopathology. Microcomputed tomography (µCT) was used to detect bone density and trabecular microstructure in vitro. The protein expression levels of Wnt3a, β-catenin and Runx2 in bone tissue were detected by Western blots.Results Zuogui Pill significantly decreased the serum level of bone alkaline phosphatase (BALP) and the level of amino terminal procollagen Ⅰ propeptide (PINP) but had no significant effect on oestradiol (E2). Zuogui Pill improved bone tissue morphology, bone microstructure and bone mineral density. The protein expression levels of Wnt3a, β-catenin and Runx2 in the Zuogui Pill groups were significantly increased.Conclusion Zuogui Pill exerts a bone-protective effect through the Wnt/β-catenin and Wnt/Runx2 pathways and has good application value for the treatment of osteoporosis.

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“…The Notch signaling pathway plays a crucial role in regulating cell fate decisions under physiological conditions, influencing cell proliferation, differentiation, development, and homeostasis. However, dysregulation of the Notch signaling pathway has been increasingly observed in various human malignancies, 54 , 55 spanning digestive system tumors, respiratory system tumors, hematological malignancies, urinary system tumors, reproductive system tumors, nervous system neoplasms, and tumors in other systems (Fig. 2 ).…”

Section: The Notch Signaling Pathway and Cancermentioning

confidence: 99%

Notch signaling pathway in cancer: from mechanistic insights to targeted therapies

Shi,

Xue,

Zeng

et al. 2024

Sig Transduct Target Ther

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Notch signaling, renowned for its role in regulating cell fate, organ development, and tissue homeostasis across metazoans, is highly conserved throughout evolution. The Notch receptor and its ligands are transmembrane proteins containing epidermal growth factor-like repeat sequences, typically necessitating receptor-ligand interaction to initiate classical Notch signaling transduction. Accumulating evidence indicates that the Notch signaling pathway serves as both an oncogenic factor and a tumor suppressor in various cancer types. Dysregulation of this pathway promotes epithelial-mesenchymal transition and angiogenesis in malignancies, closely linked to cancer proliferation, invasion, and metastasis. Furthermore, the Notch signaling pathway contributes to maintaining stem-like properties in cancer cells, thereby enhancing cancer invasiveness. The regulatory role of the Notch signaling pathway in cancer metabolic reprogramming and the tumor microenvironment suggests its pivotal involvement in balancing oncogenic and tumor suppressive effects. Moreover, the Notch signaling pathway is implicated in conferring chemoresistance to tumor cells. Therefore, a comprehensive understanding of these biological processes is crucial for developing innovative therapeutic strategies targeting Notch signaling. This review focuses on the research progress of the Notch signaling pathway in cancers, providing in-depth insights into the potential mechanisms of Notch signaling regulation in the occurrence and progression of cancer. Additionally, the review summarizes pharmaceutical clinical trials targeting Notch signaling for cancer therapy, aiming to offer new insights into therapeutic strategies for human malignancies.

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Non-coding RNAs targeting notch signaling pathway in cancer: From proliferation to cancer therapy resistance

Cited by 15 publications

References 217 publications

Celastrol can inhibit the growth of SHH medulloblastoma: In vitro and in vivo studies

Celastrol can inhibit the growth of SHH medulloblastoma: In vitro and in vivo studies

Bone protection mechanism of Zuogui Pill in an osteoporosis model of breast cancer rats after endocrine therapy

Notch signaling pathway in cancer: from mechanistic insights to targeted therapies

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