Inhibition of Survivin by Adenovirus Vector Enhanced Paclitaxel-induced Apoptosis in Breast Cancer Cells

Tanaka, Toshihiro; Uchida, Hiroaki

doi:10.21873/anticanres.12725

Cited by 6 publications

(6 citation statements)

References 16 publications

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“…Numerous research have revealed that inhibiting the c‐Myc and survivin can sensitize cancer cells to anti‐cancer drug treatment. [ 36 ] Here, crocin inhibited the c‐Myc and survivin mRNA expression levels validating the role of c‐Myc and survivin inhibition in crocin‐induced apoptosis and G1 arrest in FTC‐133 cells. Additionally, findings from a preceding investigation highlighted that the expression of these protein decreased cancer cells ability to form colonies, promote cell‐cycle inhibition at G1 phase to induce apoptosis.…”

Section: Discussionsupporting

confidence: 59%

Crocin treatment promotes the oxidative stress and apoptosis in human thyroid cancer cells FTC‐133 through the inhibition of STAT/JAK signaling pathway

Zhang

Zhu

Mohan³

et al. 2020

J Biochem & Molecular Tox

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Thyroid cancer is the most frequent endocrine malignancy, which accounts for nearly 1% of all the cancer worldwide. Crocin has a diverse biological function, such as anti‐cancer, anti‐inflammatory and antioxidant functions, specifically in the respiratory related diseases. Using in vitro techniques, this work was intended to illuminate the anti‐cancer effect of crocin in follicular thyroid carcinoma (FTC) (FT 133 cells), and the potential molecular mechanism convoluted. The outcome of the present work showed that crocin was able to prevent the proliferation and triggering the apoptosis in a dose‐dependent mode, of FTC‐133 cells by methyl thiazolyldiphenyl‐tetrazolium bromide and staining assay (acridine orange/propiduim iodide [PI], 4′,6‐diamidino‐2‐phenylindole, and PI dye). Crocin did not show toxicity to the normal thyroid (PCCL3) cells. Crocin‐induced reactive oxygen species, mitochondrial membrane potential activity, caspase‐8 and ‐9, lipid peroxidation (thiobarbituric acid reactive substances) activity while suppressing antioxidant activity (superoxide dismutase, catalase, and glutathione) in FTC‐133 cells. In addition, crocin was also participated in a halting of the proteins related to cell cycle, cyclin D1, and pro‐apoptotic proteins; Bax and caspase‐3 expression, together with the elevation of anti‐apoptotic factor Bcl‐2. Further, crocin have a dual inhibition of two major pathways, nuclear factor‐κB, extracellular signal‐regulated kinase, and janus kinase‐signal transducer and activator of transcription signaling pathways. In conclusion, crocin can inhibit follicular thyroid carcinoma proliferation and promote cell apoptosis.

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Section: Discussionsupporting

confidence: 59%

Crocin treatment promotes the oxidative stress and apoptosis in human thyroid cancer cells FTC‐133 through the inhibition of STAT/JAK signaling pathway

Zhang

Zhu

Mohan³

et al. 2020

J Biochem & Molecular Tox

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“…Interestingly, MCF-7 and MDA-MB-231 cells exposed to LQB-223 increased survivin protein levels at early time-points. Although involved in inhibition of apoptosis, survivin is an important regulator of cell cycle through interaction with chromosomal passenger proteins and stabilization of microtubules [54,55,56]. We suggest here that the increase in survivin protein levels could have a minor role in the molecular mechanisms involved in LQB-223-induced G2/M cell cycle arrest [10,57,58].…”

Section: Discussionmentioning

confidence: 99%

“…Many studies have shown that inhibition of survivin can sensitize cells to drug treatment. Downregulation of survivin enhanced paclitaxel-induced apoptosis in MCF-7 cells [56]. In MDA-MB-231 cells, survivin silencing by MX106/MX107 inhibited the oncogenic survivin function and decreased the cancer stem-like cell population, increasing drug sensitivity [59].…”

Section: Discussionmentioning

confidence: 99%

The LQB-223 Compound Modulates Antiapoptotic Proteins and Impairs Breast Cancer Cell Growth and Migration

Lemos

Longo

Mendonça

et al. 2019

IJMS

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Drug resistance represents a major issue in treating breast cancer, despite the identification of novel therapeutic strategies, biomarkers, and subgroups. We have previously identified the LQB-223, 11a-N-Tosyl-5-deoxi-pterocarpan, as a promising compound in sensitizing doxorubicin-resistant breast cancer cells, with little toxicity to non-neoplastic cells. Here, we investigated the mechanisms underlying LQB-223 antitumor effects in 2D and 3D models of breast cancer. MCF-7 and MDA-MB-231 cells had migration and motility profile assessed by wound-healing and phagokinetic track motility assays, respectively. Cytotoxicity in 3D conformation was evaluated by measuring spheroid size and performing acid phosphatase and gelatin migration assays. Protein expression was analyzed by immunoblotting. Our results show that LQB-223, but not doxorubicin treatment, suppressed the migratory and motility capacity of breast cancer cells. In 3D conformation, LQB-223 remarkably decreased cell viability, as well as reduced 3D culture size and migration. Mechanistically, LQB-223-mediated anticancer effects involved decreased proteins levels of XIAP, c-IAP1, and Mcl-1 chemoresistance-related proteins, but not survivin. Survivin knockdown partially potentiated LQB-223-induced cytotoxicity. Additionally, cell treatment with LQB-223 resulted in changes in the mRNA levels of epithelial-mesenchymal transition markers, suggesting that it might modulate cell plasticity. Our data demonstrate that LQB-223 impairs 3D culture growth and migration in 2D and 3D models of breast cancer exhibiting different phenotypes.

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“…The most common low CAR cancer cell lines, including CT26, 4T1, and MCF7, were widely used in establishing tumor models for cancer immunotherapy [32][33][34]. However, these cell lines have not yet been extensively studied in vivo for adenoviral therapy due to poor infectivity in vitro [35][36][37][38]. To overcome this issue of poor infectivity, the liposome-encapsulated adenovirus platform was developed to transduce low CAR cells efficiently in vitro [24,39,40] In a previous study using a small number of mice, DOTAP-Folate liposomes encapsulated TAV255, produced by the sonication technique, efficiently treated CT26 tumors and significantly increased the population of tumor-infiltrating cytotoxic T cells.…”

Section: Introductionmentioning

confidence: 99%

A Local and Abscopal Effect Observed with Liposomal Encapsulation of Intratumorally Injected Oncolytic Adenoviral Therapy

Dong

Shah

Phung

et al. 2023

Cancers

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This study evaluated the in vivo therapeutic efficacy of oncolytic serotype 5 adenovirus TAV255 in CAR-deficient tumors. In vitro experiments were performed with cell lines that expressed different levels of CAR (HEK293, A549, CT26, 4T1, and MCF-7). Low CAR cells, such as CT26, were poorly transduced by Ad in vitro unless the adenovirus was encapsulated in liposomes. However, the CT26 tumor in an immune-competent mouse model responded to the unencapsulated TAV255; 33% of the tumors were induced into complete remission, and mice with complete remission rejected the rechallenge with cancer cell injection. Encapsulation of TAV255 improves its therapeutic efficacy by transducing more CT26 cells, as expected from in vitro results. In a bilateral tumor model, nonencapsulated TAV255 reduced the growth rate of the locally treated tumors but had no effect on the growth rate of the distant tumor site. Conversely, encapsulated TAV255-infected CT26 induced a delayed growth rate of both the primary injected tumor and the distant tumor, consistent with a robust immune response. In vivo, intratumorally injected unencapsulated adenoviruses infect CAR-negative cells with only limited efficiency. However, unencapsulated adenoviruses robustly inhibit the growth of CAR-deficient tumors, an effect that constitutes an ‘in situ vaccination’ by stimulating cytotoxic T cells.

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Inhibition of Survivin by Adenovirus Vector Enhanced Paclitaxel-induced Apoptosis in Breast Cancer Cells

Abstract: Loss of survivin expression enhanced paclitaxel-induced apoptosis in MCF-7 breast cancer cells in vitro.

Cited by 6 publications

References 16 publications

Crocin treatment promotes the oxidative stress and apoptosis in human thyroid cancer cells FTC‐133 through the inhibition of STAT/JAK signaling pathway

Crocin treatment promotes the oxidative stress and apoptosis in human thyroid cancer cells FTC‐133 through the inhibition of STAT/JAK signaling pathway

The LQB-223 Compound Modulates Antiapoptotic Proteins and Impairs Breast Cancer Cell Growth and Migration

A Local and Abscopal Effect Observed with Liposomal Encapsulation of Intratumorally Injected Oncolytic Adenoviral Therapy

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