Tumor-penetrating iRGD facilitates penetration of poly(floxuridine-ketal)-based nanomedicine for enhanced pancreatic cancer therapy

Li, Xingwei; Zhong, Haiping; Zheng, Shujing; Mu, Jingqing; Yu, Na; Guo, Shutao

doi:10.1016/j.jconrel.2024.04.004

Cited by 5 publications

(2 citation statements)

References 44 publications

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“…And the tumor-penetrating peptide triggered the endocytosis function within the tumor cells successfully improved the nanomedicine penetration in the tumor. 121 Poly(2-(N-oxide-N, N-diethylamino)ethyl methacrylate) (PODEA) is a zwitterionic polymer that shows a high affinity for the cell membrane and can trigger the endocytic mechanism. Yu et al conjugated this fragment to multifunctional nanoparticles loaded with FAK inhibitor, Sting activator, and chemotherapy drug, and delivered the multifunctional nanoparticles deep into the tumor, realizing the combination of stroma remodeling with immunotherapy and chemotherapy.…”

Section: Molecularmentioning

confidence: 99%

“…simultaneously administered a prodrug nanoparticle of the cytotoxic drug floxuridine with a tumor-penetrating peptide. And the tumor-penetrating peptide triggered the endocytosis function within the tumor cells successfully improved the nanomedicine penetration in the tumor . Poly(2-(N-oxide-N, N-diethylamino)ethyl methacrylate) (PODEA) is a zwitterionic polymer that shows a high affinity for the cell membrane and can trigger the endocytic mechanism.…”

Section: Integration Of Stromal Remodeling With Anti-tumor Treatment ...mentioning

confidence: 99%

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Breaking Down Barriers in Drug Delivery by Stromal Remodeling Approaches in Pancreatic Cancer

Zhou,

Ma,

Sheng

et al. 2024

Mol. Pharmaceutics

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Pancreatic cancer remains a formidable challenge in oncology due to its aggressive nature and limited treatment options. The dense stroma surrounding pancreatic tumors not only provides structural support but also presents a formidable barrier to effective therapy, hindering drug penetration and immune cell infiltration. This review delves into the intricate interplay between stromal components and cancer cells, highlighting their impact on treatment resistance and prognosis. Strategies for stromal remodeling, including modulation of cancerassociated fibroblasts (CAFs), pancreatic stellate cells (PSCs) activation states, and targeting extracellular matrix (ECM) components, are examined for their potential to enhance drug penetration and improve therapeutic efficacy. Integration of stromal remodeling with conventional therapies, such as chemotherapy and immunotherapy, is discussed along with the emerging field of intelligent nanosystems for targeted drug delivery. This comprehensive overview underscores the importance of stromal remodeling in pancreatic cancer treatment and offers insights into promising avenues for future research and clinical translation.

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Section: Molecularmentioning

confidence: 99%

Section: Integration Of Stromal Remodeling With Anti-tumor Treatment ...mentioning

confidence: 99%

Breaking Down Barriers in Drug Delivery by Stromal Remodeling Approaches in Pancreatic Cancer

Zhou,

Ma,

Sheng

et al. 2024

Mol. Pharmaceutics

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PLGA‐PEG‐c(RGDfK)‐Kushenol E Micelles With a Therapeutic Potential for Targeting Ovarian Cancer

Chen,

Wan,

et al. 2024

IET Nanobiotechnology

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Background: As a naturally derived inhibitor of autophagy, Kushenol E (KE) is a biprenylated flavonoid and is isolated from Sophora flavescens, which has been used for the treatment of cancer, hepatitis, and skin diseases. However, KE, as a poorly soluble drug, exhibited strong autophagy regulating activity in in vitro cancer cell lines, but no related studies have reported its antiovarian cancer property. Therefore, it is very beneficial to enhance the antineoplastic properties of KE by establishing an ovarian tumor‐targeting nanoparticle system modified with tumor‐homing c(RGDfK) peptides.Materials and Methods: In the current study, poly(lactic‐co‐glycolic acid)‐poly(ethylene glycol)‐modified with cyclic RGDfK peptide (PLGA‐PEG‐c(RGDfK))‐KE micelles (PPCKM) were prepared to overcome the poor water solubility of KE to meet the requirement of tumor‐active targeting. The effect of PPCKM on ovarian cancer was evaluated on SKOV‐3 cells and xenograft models in BALB/c nude mice.Results: The PPCKM showed a higher drug cumulative release ratio (82.16 ± 7.69% vs. 34.96 ± 3.05%, at 1.5 h) with good morphology, particle size (93.41 ± 2.84 nm), and entrapment efficiency (89.7% ± 1.3%). The cell viability, migration, and apoptosis analysis of SKOV‐3 cells demonstrated that PPCKM retained potent antitumor effects and promoted apoptosis at early and advanced stages with concentration‐dependent. Based on the establishment of xenograft models in BALB/c nude mice, we discovered that PPCKM reduced tumor volume and weight, inhibited proliferating cell nuclear antigen (PCNA) and Ki67 expression, as well as promoted apoptosis by targeting the tumor site.Conclusion: The findings in this study suggest that PPCKM may serve as an effective therapeutic option for ovarian cancer.

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Branched oncolytic peptides target HSPGs, inhibit metastasis, and trigger the release of molecular determinants of immunogenic cell death in pancreatic cancer

Rencinai,

Tollapi,

Marianantoni

et al. 2024

Front. Mol. Biosci.

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Immunogenic cell death (ICD) can be exploited to treat non-immunoreactive tumors that do not respond to current standard and innovative therapies. Not all chemotherapeutics trigger ICD, among those that do exert this effect, there are anthracyclines, irinotecan, some platinum derivatives and oncolytic peptides. We studied two new branched oncolytic peptides, BOP7 and BOP9 that proved to elicit the release of damage-associated molecular patterns DAMPS, mediators of ICD, in pancreatic cancer cells. The two BOPs selectively bound and killed tumor cells, particularly PANC-1 and Mia PaCa-2, but not cells of non-tumor origin such as RAW 264.7, CHO-K1 and pgsA-745. The cancer selectivity of the two BOPs may be attributed to their repeated cationic sequences, which enable multivalent binding to heparan sulfate glycosaminoglycans (HSPGs), bearing multiple anionic sulfation patterns on cancer cells. This interaction of BOPs with HSPGs not only fosters an anti-metastatic effect in vitro, as demonstrated by reduced adhesion and migration of PANC-1 cancer cells, but also shows promising tumor-specific cytotoxicity and low hemolytic activity. Remarkably, the cytotoxicity induced by BOPs triggers the release of DAMPs, particularly HMGB1, IFN-β and ATP, by dying cells, persisting longer than the cytotoxicity of conventional chemotherapeutic agents such as irinotecan and daunorubicin. An in vivo assay in nude mice showed an encouraging 20% inhibition of tumor grafting and growth in a pancreatic cancer model by BOP9.

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Tumor-penetrating iRGD facilitates penetration of poly(floxuridine-ketal)-based nanomedicine for enhanced pancreatic cancer therapy

Cited by 5 publications

References 44 publications

Breaking Down Barriers in Drug Delivery by Stromal Remodeling Approaches in Pancreatic Cancer

Breaking Down Barriers in Drug Delivery by Stromal Remodeling Approaches in Pancreatic Cancer

PLGA‐PEG‐c(RGDfK)‐Kushenol E Micelles With a Therapeutic Potential for Targeting Ovarian Cancer

Branched oncolytic peptides target HSPGs, inhibit metastasis, and trigger the release of molecular determinants of immunogenic cell death in pancreatic cancer

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