Targeting strategies of adenovirus-mediated gene therapy and virotherapy for prostate cancer

Cai, Zhonglin; Lv, Haidi; Cao, Wenjuan; Zhou, Chuan; Liu, Qiangzhao; Li, Hui; Zhou, Fenghai

doi:10.3892/mmr.2017.7487

Cited by 14 publications

(10 citation statements)

References 117 publications

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“…Gene therapy has brought about a breakthrough for the treatment of prostate cancer, and a number of studies have identified a substantial number of genes that may be potential targets for the treatment of this malignancy (11,12). In the present study, AIPC cell lines PC3 and DU145, which do not respond to androgens, glucocorticoids or epidermal/fibroblast growth factors, were selected as models (13,14). In addition, the cisplatin-resistant subline of PC3, PC3/DDP, was used.…”

Section: Introductionmentioning

confidence: 99%

Reduced pim‑1 expression increases chemotherapeutic drug sensitivity in human androgen‑independent prostate cancer cells by inducing apoptosis

et al. 2019

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Chemotherapeutic drug resistance is an obstacle for the successful therapy of prostate cancer. The aim of the present study was to identify the effects of proto-oncogene serine/threonine-protein kinase pim-1 (pim-1) in the proliferation of chemotherapeutic drug-resistant prostate cancer cells. Androgen-independent human prostate cancer cell lines PC3 and DU145 were used in the current study. Cisplatin-sensitive PC3 cells and cisplatin-resistant PC3/DDP cells were used in drug-resistance assays. The expression levels of pim-1, permeability glycoprotein (p-gp), caspase-3 and cleaved caspase-3 were determined using western blotting analysis; pim-1 was knocked down using pim-1-specific short hairpin RNA (shRNA); cell viability was determined using MTT assay and IC 50 values of the chemotherapeutic drugs in human prostate cancer cells tested were calculated using GraphPad 5 software. Androgen-independent human prostate cancer cell lines PC3 and DU145 were transfected with pim-1-targeted or control shRNA, and MTT results revealed that pim-1 knockdown significantly inhibited PC3 and DU145 cell viability in a time-dependent manner (P<0.01). Cisplatin-resistant cells PC3/DDP exhibited higher levels of pim-1 and p-gp expression compared with cisplatin-sensitive PC3 cells; and pim-1 knockdown markedly increased chemotherapeutic drug sensitivity in PC3/DDP cells. In addition, pim-1 knockdown increased chemotherapeutic drug sensitivity in PC3/DDP cells. The molecular mechanism of drug sensitivity was discovered to be partly due to pim-1 knockdown, as it significantly increased apoptosis in cisplatin-resistant PC3/DDP cells. The present study may provide a new strategy for the therapy of prostate cancer.

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Section: Introductionmentioning

confidence: 99%

Reduced pim‑1 expression increases chemotherapeutic drug sensitivity in human androgen‑independent prostate cancer cells by inducing apoptosis

et al. 2019

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“…Development of effective PCa gene therapies was the objective of many research groups and numerous publications detail their findings (e.g. [56][57][58][59][60][61]. Some gene therapies (e.g.…”

Section: Discussionmentioning

confidence: 99%

Personalized 1-2-3-Gene(s) Tickets to Cancer-Free Prostate

Iacobaş¹,

Iacobaş²

2021

Preprint

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Many years and $$$ spent for research did not yet produced a universally effective gene therapy of prostate cancer (PCa). Our studies indicated that not only each human, but even each cancer nodule in the same tumor has unique and dynamic gene expression profile, control and coordination. The tumor heterogeneity of the transcriptome topology is a strong argument in favor of personalized gene therapies, tailored on patients’ primary tumor unique characteristics. Here, we propose a bioinformatics procedure by which to identify the Gene Master Regulators (GMR) of cancer cells from transcriptomic data and predict consequences of their experimental manipulation. The procedure, based on our Genomic Fabric Paradigm (GFP), can determine the most important gene in each cancer nodule whose controlled alteration would selectively kill the cancer cells. In this report, the method is applied to our microarray data on two men PCs (each with three distinct cancer nodules) and two standard human PCa cell lines (DU145 and LNCaP). We expect the industry to produce ready-to-use CRISPR constructs for all genes allowing the clinical oncologist to prescribe the adequate personalized CRISPR cocktail for his/her patient. Thus, the GMR approach may provide the most effective, yet affordable solution in fighting cancer.

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“…There are five early transcription units (E1A, E1B, E2, E3 and E4), two delayed transcription units (IX and Iva2) and one late transcription unit (L1-L5) in Ad 5 coding region [7]. E1A conserved region 2 (E1A-CR2) interacts with retinoblastoma (Rb) in host cells to promote S-phase entry and viral DNA replication [7]. E1B contains E1B-19K and E1B-55K.…”

Section: Genome Structure Of Admentioning

confidence: 99%

Tropism and transduction of oncolytic adenovirus vectors in prostate cancer therapy

Wei

et al. 2021

Front. Biosci. (Landmark Ed)

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Oncolytic adenovirus has been applied in cancer therapy because of several advantages such as cost-effective production, high transduction efficiency and low toxicity. Recent efforts have been focused on the modification of oncolytic adenovirus by encoding transgenes within the viral genome to efficiently and selectively replicate within cancer cells, destroy cancerous cells, induce tumor cell apoptosis, and stimulate the recruitment of immune cells to the tumor site. Nevertheless, there are still big challenges for translational research of oncolytic virotherapy in clinical cancer management. Therefore, here we summarize current status on the design and application of oncolytic adenovirus vectors for prostate cancer therapy. In particular, we describe the main receptors associated with the tropism and transduction of oncolytic adenovirus vectors, and propose new directions in future studies for prostate cancer virotherapy.

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Targeting strategies of adenovirus-mediated gene therapy and virotherapy for prostate cancer

Cited by 14 publications

References 117 publications

Reduced pim‑1 expression increases chemotherapeutic drug sensitivity in human androgen‑independent prostate cancer cells by inducing apoptosis

Reduced pim‑1 expression increases chemotherapeutic drug sensitivity in human androgen‑independent prostate cancer cells by inducing apoptosis

Personalized 1-2-3-Gene(s) Tickets to Cancer-Free Prostate

Tropism and transduction of oncolytic adenovirus vectors in prostate cancer therapy

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