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    Long noncoding RNAs (lncRNAs) in pancreatic cancer progression
    (Elsevier Science, 2022) Ashrafizadeh, Milad; Rabiee, Navid; Prem Kumar, Alan; Sethi, Gautam; Zarrabi, Ali; Wang, Yuzhuo
    Long noncoding RNAs (lncRNAs) are RNA molecules involved in gene regulation at transcriptional, post-transcriptional, and epigenetic levels. lncRNAs participate in regulating apoptosis and autophagy in pancreatic cancer (PCa) and can promote and/or decrease the proliferation rate of tumor cells. The metastasis of PCa cells is tightly regulated by lncRNAs and they can affect the mechanism of epithelial-mesenchymal transition (EMT) to modulate metastasis. The drug resistance of PCa cells, especially to gemcitabine, can be affected by lncRNAs. In addition, lncRNAs enriched in exosomes can be transferred among tumor cells to regulate their proliferation and metastasis. Antitumor compounds, such as curcumin and ginsenosides, can regulate lncRNA expression in PCa therapy. As we discuss here, the expression level of lncRNAs can be considered as both a diagnostic and prognostic tool in patients with PCa. Teaser: We discuss the role of long noncoding RNAs in the proliferation, invasion, and therapy response of pancreatic cancer cells, evaluating their prognostic and diagnostic functions in the clinical course of this disease.
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    Micelle-engineered nanoplatforms for precision oncology
    (Elsevier science, 2024) Gao, Wei; Bigham, Ashkan; Ghomi, Matineh; Zarrabi, Ali; Rabiee, Navid; Saeb, Mohammad Reza; Ertaş, Yavuz Nuri; Goel, Arul; Sharifi, Esmaeel; Ashrafizadeh, Milad; Sethi, Gautam; Tambuwala, Murtaza M.; Wang, Yuzhuo; Ghaffarlou, Mohammadreza; Jiao, Taiwei
    The alliance between nanomaterials and cancer therapy has revolutionized the treatment of tumor patients. After cardiovascular diseases, cancer is the leading cause of death, so interdisciplinary approaches should be used for the treatment of this malignant disease. Both treatment and early diagnosis of cancer are challenging. The micelles belong to lipid-based nanostructures, and they have a hydrophobic core with hydrophilic head regions. The current review article focuses on the application of micelles in cancer suppression. The micelles can provide a platform for co-delivery of non-coding RNAs and RNAi in cancer gene therapy. Both synthetic and natural
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    NF-?B as a regulator of cancer metastasis and therapy response: A focus on epithelial-mesenchymal transition
    (Wiley, 2022) Mirzaei , Sepideh; Saghari, Sam; Bassiri, Farzaneh; Raesi, Rasoul; Zarrabi, Ali; Hushmandi, Kiavash; Sethi, Gautam; Tergaonkar, Vinay
    Metastasis of tumor cells is a complex challenge and significantly diminishes theoverall survival and prognosis of cancer patients. The epithelial?to?mesenchymaltransition (EMT) is a well?known mechanism responsible for the invasiveness oftumor cells. A number of molecular pathways can regulate the EMT mechanism incancer cells and nuclear factor?kappaB (NF??B) is one of them. The nucleartranslocation of NF??B p65 can induce the transcription of several genes involved inEMT induction. The present review describes NF??B and EMT interaction in cancercells and their association in cancer progression. Due to the oncogenic role NF??Bsignaling, its activation enhances metastasis of tumor cells via EMT induction. Thishas been confirmed in various cancers including brain, breast, lung and gastriccancers, among others. The ZEB1/2, transforming growth factor??, and Slug asinducers of EMT undergo upregulation by NF??B to promote metastasis of tumorcells. After EMT induction driven by NF??B, a significant decrease occurs inE?cadherin levels, while N?cadherin and vimentin levels undergo an increase. Thenoncoding RNAs can potentially also function as upstream mediators and modulateNF??B/EMT axis in cancers. Moreover, NF??B/EMT axis is involved in mediatingJ Cell Physiol. 2022;1–26.wileyonlinelibrary.com/journal/jcp© 2022 Wiley Periodicals LLC.|1Abbreviations:AREG, amphiregulin; circRNA, circular RNA; DLC?1, deleted in liver cancer?1; EMT, epithelial?to?mesenchymal transition; EMT?TFs, EMT?inducing transcription factors;FABP5, fatty acid?binding protein 5; GH, growth hormone; IGF1R, insulin like growth factor?1 receptor; IKK, I?B kinase; IL, interleukin; lncRNA, long noncoding RNA; MANF, mesencephalicastrocyte?derived neutrophic factor; miRNA, microRNA; NF??B, nuclear factor?kappaB; NIK, NF??B inducing kinase; SIRTs, sirtuins; SMC4, structural maintenance of chromosome 4;STAT3, signal transducer and activator of transcription 3; TGF??, transforming growth factor??; TLR?4, toll like growth factor?4; TNF, tumor necrosis factor. drug resistance in tumor cells. Thus, suppressing NF??B/EMT axis can also promotethe sensitivity of cancer cells to chemotherapeutic agents
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    Non-coding RNA-based regulation of inflammation
    (Elsevier Science, 2022) Ashrafizadeh, Milad; Zarrabi, Ali; Mostafavi, Ebrahim; Aref, Amir Reza; Sethi, Gautam; Wang, Lingzhi; Tergaonkar, Vinay
    nflammation is a multifactorial process and various biological mechanisms and pathways participate in its development. The presence of inflammation is involved in pathogenesis of different diseases such as diabetes mellitus, cardiovascular diseases and even, cancer. Non-coding RNAs (ncRNAs) comprise large part of tran- scribed genome and their critical function in physiological and pathological conditions has been confirmed. The present review focuses on miRNAs, lncRNAs and circRNAs as ncRNAs and their potential functions in inflam- mation regulation and resolution. Pro-inflammatory and anti-inflammatory factors are regulated by miRNAs via binding to 3’-UTR or indirectly via affecting other pathways such as SIRT1 and NF-?B. LncRNAs display a similar function and they can also affect miRNAs via sponging in regulating levels of cytokines. CircRNAs mainly affect miRNAs and reduce their expression in regulating cytokine levels. Notably, exosomal ncRNAs have shown ca- pacity in inflammation resolution. In addition to pre-clinical studies, clinical trials have examined role of ncRNAs in inflammation-mediated disease pathogenesis and cytokine regulation. The therapeutic targeting of ncRNAs using drugs and nucleic acids have been analyzed to reduce inflammation in disease therapy. Therefore, ncRNAs
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    Non-coding RNAs and macrophage interaction in tumor progression
    (Elsevier Ireland Ltd, 2022) Entezari, Maliheh; Sadrkhanloo, Mehrdokht; Rashidi, Mohsen; Asnaf, Sholeh Etehad; Taheriazam, Afshin; Hashemi, Mehrdad; Ashrafizadeh, Milad; Zarrabi, Ali; Rabiee, Navid; Hushmandi, Kiavash; Mirzaei, Sepideh; Sethi, Gautam
    The macrophages are abundantly found in TME and their M2 polarization is in favor of tumor malignancy. On the other hand, non-coding RNAs (ncRNAs) can modulate macrophage polarization in TME to affect cancer progression. The miRNAs can dually induce/suppress M2 polarization of macrophages and by affecting various molecular pathways, they modulate tumor progression and therapy response. The lncRNAs can affect miRNAs via sponging and other molecular pathways to modulate macrophage polarization. A few experiments have also examined role of circRNAs in targeting signaling networks and affecting macrophages. The therapeutic targeting of these ncRNAs can mediate TME remodeling and affect macrophage polarization. Furthermore, exosomal ncRNAs derived from tumor cells or macrophages can modulate polarization and TME remodeling. Suppressing biogenesis and secretion of exosomes can inhibit ncRNA-mediated M2 polarization of macrophages and prevent tumor progression. The ncRNAs, especially exosomal ncRNAs can be considered as non-invasive biomarkers for tumor diagnosis. © 2022 Elsevier B.V.
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    Noncoding RNAs as regulators of STAT3 pathway in gastrointestinal cancers: Roles in cancer progression and therapeutic response
    (Wiley, 2023) Ashrafizadeh, Milad; Mohan, Chakrabhavi D.; Rangappa, Shobith; Zarrabi, Ali; Hushmandi, Kiavash; Kumar, Alan Prem; Sethi, Gautam
    Gastrointestinal (GI) tumors (cancers of the esophagus, gastric, liver, pancreas, colon, and rectum) contribute to a large number of deaths worldwide. STAT3 is an oncogenic transcription factor that promotes the transcription of genes associated with proliferation, antiapoptosis, survival, and metastasis. STAT3 is overactivated in many human malignancies including GI tumors which accelerates tumor progression, metastasis, and drug resistance. Research in recent years demonstrated that noncoding RNAs (ncRNAs) play a major role in the regulation of many signaling pathways including the STAT3 pathway. The major types of endogenous ncRNAs that are being extensively studied in oncology are microRNAs, long noncoding RNAs, and circular RNAs. These ncRNAs can either be tumor-promoters or tumor-suppressors and each one of them imparts their activity via different mechanisms. The STAT3 pathway is also tightly modulated by ncRNAs. In this article, we have elaborated on the tumor-promoting role of STAT3 signaling in GI tumors. Subsequently, we have comprehensively discussed the oncogenic as well as tumor suppressor functions and mechanism of action of ncRNAs that are known to modulate STAT3 signaling in GI cancers.
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    Wnt/?-Catenin signaling as a driver of hepatocellular carcinoma progression: an emphasis on molecular pathways
    (Dove Medical Press, 2021) Deldar Abad Paskeh, Mahshid; Mirzaei, Sepideh; Ashrafizadeh, Milad; Zarrabi, Ali; Sethi, Gautam
    Liver cancers cause a high rate of death worldwide and hepatocellular carcinoma (HCC) is considered as the most common primary liver cancer. HCC remains a challenging disease to treat. Wnt/?-catenin signaling pathway is considered a tumor-promoting factor in various cancers; hence, the present review focused on the role of Wnt signaling in HCC, and its association with progression and therapy response based on pre-clinical and clinical evidence. The nuclear translocation of ?-catenin enhances expression level of genes such as c-Myc and MMPs in increasing cancer progression. The mutation of CTNNB1 gene encoding ?-catenin and its overexpression can lead to HCC progression. ?-catenin signaling enhances cancer stem cell features of HCC and promotes their growth rate. Furthermore, ?-catenin prevents apoptosis in HCC cells and increases their migration via triggering EMT and upregulating MMP levels. It is suggested that ?-catenin signaling participates in mediating drug resistance and immuno-resistance in HCC. Upstream mediators including ncRNAs can regulate ?-catenin signaling in HCC. Anti-cancer agents inhibit ?-catenin signaling and mediate its proteasomal degradation in HCC therapy. Furthermore, clinical studies have revealed the role of ?-catenin and its gene mutation (CTNBB1) in HCC progression. Based on these subjects, future experiments can focus on developing novel therapeutics targeting Wnt/?-catenin signaling in HCC therapy.