siRNA and targeted delivery systems in breast cancer therapy

Mirzaei, Sepideh; Paskeh, Mahshid Deldar Abad; Entezari, Maliheh; Bidooki, Seyed Hesamoddin; Ghaleh, Vahideh Javadian; Rezaei, Shamin; Hejazi, Elahe Sadat; Kakavand, Amirabbas; Behroozaghdam, Mitra; Movafagh, Abolfazl; Taheriazam, Afshin; Hashemi, Mehrdad; Samarghandian, Saeed

doi:10.1007/s12094-022-03043-y

Cited by 8 publications

(5 citation statements)

References 250 publications

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“…Treatment with the Notch1 monoclonal antibody bronticuzumab could delay ACC progression and contribute to partial reduction of tumor volume 27 , 28 . siRNA targeting Notch1 significantly reduces Notch1 expression, thereby inhibiting tumor cell proliferation and migration, inducing cell apoptosis, and exhibiting anticancer effects 29 , 30 . Among these approaches, research has focused on γ-secretase inhibitors (GSIs), which exert promising anticancer effects when used alone or in combination with other anticancer drugs 31 .…”

Section: Discussionmentioning

confidence: 99%

Targeting the ZMIZ1-Notch1 signaling axis for the treatment of tongue squamous cell carcinoma

Pang,

Sun,

et al. 2024

Sci Rep

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Zinc finger MIZ-type containing 1 (ZMIZ1) is a transcriptional coactivator related to the protein inhibitors of activated STATs (PIAS) family. Mounting evidence suggests that ZMIZ1 plays a crucial role in the occurrence and development of cancers. The function of ZMIZ1 in tongue squamous cell carcinoma (TSCC) and the mechanisms underpinning its role in this disease have not been fully clarified. We performed qualitative ZMIZ1 protein expression analyses using immunohistochemistry in 20 patient-derived, paraffin-embedded TSCC tissue sections. We used RNAi to knock down ZMIZ1 expression in the CAL-27 TSCC cell line and quantified the impact of ZMIZ1 knock down on proliferation, migration and apoptosis via CCK-8, scratch assay and flow cytometry, respectively. We used qRT-PCR and western blotting to investigate the role of ZMIZ1 in this cell line. Finally, we established a model of lung metastasis in nude mice to replicate the in vitro results. ZMIZ1 protein was significantly more abundant in TSCC case tissue samples. ZMIZ1 knockdown reduced the invasion and metastases of TSCC tumor cells and promoted apoptosis. ZMIZ1 knockdown was associated with the down-regulation of Notch signaling pathway related factors Jagged1 and Notch1, and invasion and metastasis related factors MKP-1, SSBP2 and MMP7 in vitro and in vivo, at the mRNA level. In vitro and in vivo data suggest that knock down of ZMIZ1 may inhibit TSCC invasion and metastasis by modulating Notch signaling. ZMIZ1 inhibition may therefore represent a new therapeutic target for TSCC.

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Section: Discussionmentioning

confidence: 99%

Targeting the ZMIZ1-Notch1 signaling axis for the treatment of tongue squamous cell carcinoma

Pang,

Sun,

et al. 2024

Sci Rep

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“…Cont. Apoptotic pathways 1,4,7,26 Proteasome-mediated degradation 2,10 Protein kinase binding 3,27 Protein disulfide isomerase activity 5 Unfolded protein response 6,13,28 Cellular responses to stimuli 6,11,13,29 Regulation of actin dynamics for phagocytic cup formation 8 Plasma lipoprotein assembly, remodeling, and clearance 9 PERK regulates gene expression 11,29 Translational control 12 Signaling receptor activity 14 Metabolism of proteins 15,16,23,24 Regulation of degradation 17 MIF-mediated glucocorticoid regulation 18,26 Prolactin signaling 19 Homology directed repair 20 DNA double strand break response 20 Gene expression 21,28 Endocytosis 22 Galactose metabolism 25 Vesicle trafficking 30 Processing of capped intron-containing pre-mRNA 31 [137,[139][140][141][142][143][144][145][146][147][148][149][150][151] Esophageal squamous cell KCNH2 Potassium channels [155] Endothelial cell YAP1 Gene expression [158] Pancreas NR4A1 1 , CTNNB1 2 Gene expression 1,2 Phosphorylation 2…”

Section: Txndc5 and Other Types Of Cancermentioning

confidence: 99%

“…Unfolded protein response 1,2,5,7,8 Cellular responses to stimuli 1,5,8,19 Processing of secretory proteins 3 Translation of structural proteins 4 Proteasome-mediated degradation 6,16 Response to elevated platelet cytosolic Ca 2+ 7 Signaling by Rho GTPases 9 Translational control 10 Apoptotic pathways 11,12 MIF-mediated glucocorticoid regulation 11,12,13,17,18 Processing of capped intron-containing pre-mRNA 14 Selective autophagy 14 Plasma lipoprotein assembly, remodeling, and clearance 15 Gene expression 19 [40,[166][167][168][173][174][175][176] Table 4. Cont.…”

Section: Txndc5 and Heart Diseasesmentioning

confidence: 99%

“…Disulfide bonds are introduced into the nascent polypeptide outside the ribosome exit site through a dithiol-disulfide exchange reaction with the assistance of oxidoreductases, including TXNDC5 and other members of the PDI family [7,8]. The abnormal expression of TXNDC5 and single nucleotide polymorphisms (SNPs) in the TXNDC5 gene have been found to be associated with the risk of various diseases, including organ fibrosis (affecting approximately 25% of the global population) [9], atherosclerosis (causes 17.9 million deaths per year) [10], diabetes (affects approximately 463 million adults globally) [11], liver disease (causes over 2 million deaths annually worldwide) [12,13], rheumatoid arthritis (RA) (affects 0.24% of the global population) [14], cancer (an estimated 19.3 million new cancer cases and 10 million cancer deaths worldwide in 2020) [15,16], neurodegenerative disease (an estimated 50 million people worldwide) [17], and vitiligo (affects between 0.5% to 2% of the global population) [18]. TXNDC5 expression is induced under hypoxic conditions in disease states, such as RA, non-small cell lung cancer, and colorectal cancer, and also enhanced expression of TXNDC5 promotes the redox-sensitive activation of cardiac fibroblasts and the augmentation of cardiac fibrosis [1,2,4].…”

Section: Introductionmentioning

confidence: 99%

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Thioredoxin Domain Containing 5 (TXNDC5): Friend or Foe?

Bidooki,

Navarro,

Fernandes

et al. 2024

CIMB

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This review focuses on the thioredoxin domain containing 5 (TXNDC5), also known as endoplasmic reticulum protein 46 (ERp46), a member of the protein disulfide isomerase (PDI) family with a dual role in multiple diseases. TXNDC5 is highly expressed in endothelial cells, fibroblasts, pancreatic β-cells, liver cells, and hypoxic tissues, such as cancer endothelial cells and atherosclerotic plaques. TXNDC5 plays a crucial role in regulating cell proliferation, apoptosis, migration, and antioxidative stress. Its potential significance in cancer warrants further investigation, given the altered and highly adaptable metabolism of tumor cells. It has been reported that both high and low levels of TXNDC5 expression are associated with multiple diseases, such as arthritis, cancer, diabetes, brain diseases, and infections, as well as worse prognoses. TXNDC5 has been attributed to both oncogenic and tumor-suppressive features. It has been concluded that in cancer, TXNDC5 acts as a foe and responds to metabolic and cellular stress signals to promote the survival of tumor cells against apoptosis. Conversely, in normal cells, TXNDC5 acts as a friend to safeguard cells against oxidative and endoplasmic reticulum stress. Therefore, TXNDC5 could serve as a viable biomarker or even a potential pharmacological target.

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“…These findings suggest that LNPs conjugated with doxorubicin could serve as a platform for co-delivering nucleic acids and chemotherapy drugs in combination cancer therapies [158]. Since overexpression of Bcl-2 occurs in breast tumour leading to increased survival rate, the investigated system was presented as a potential tool for BC therapy [159]. Based on the discussed results it is expected that the LNPs-siRNA technology will be increasingly applied for BC treatment and have outlets in clinical practice with enormous benefits for the patients.…”

Section: Lnps For Sirna Deliverymentioning

confidence: 99%

Lipid nanoparticles-based RNA therapies for breast cancer treatment

Serpico,

Zhu,

Maia

et al. 2024

Drug Deliv. and Transl. Res.

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Breast cancer (BC) prevails as a major burden on global healthcare, being the most prevalent form of cancer among women. BC is a complex and heterogeneous disease, and current therapies, such as chemotherapy and radiotherapy, frequently fall short in providing effective solutions. These treatments fail to mitigate the risk of cancer recurrence and cause severe side effects that, in turn, compromise therapeutic responses in patients. Over the last decade, several strategies have been proposed to overcome these limitations. Among them, RNA-based technologies have demonstrated their potential across various clinical applications, notably in cancer therapy. However, RNA therapies are still limited by a series of critical issues like off-target effect and poor stability in circulation. Thus, novel approaches have been investigated to improve the targeting and bioavailability of RNA-based formulations to achieve an appropriate therapeutic outcome. Lipid nanoparticles (LNPs) have been largely proven to be an advantageous carrier for nucleic acids and RNA. This perspective explores the most recent advances on RNA-based technology with an emphasis on LNPs’ utilization as effective nanocarriers in BC therapy and most recent progresses in their clinical applications. Graphical Abstract

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siRNA and targeted delivery systems in breast cancer therapy

Cited by 8 publications

References 250 publications

Targeting the ZMIZ1-Notch1 signaling axis for the treatment of tongue squamous cell carcinoma

Targeting the ZMIZ1-Notch1 signaling axis for the treatment of tongue squamous cell carcinoma

Thioredoxin Domain Containing 5 (TXNDC5): Friend or Foe?

Lipid nanoparticles-based RNA therapies for breast cancer treatment

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