Expression of cyclin A, B1 and D1 after induction of cell cycle arrest in the Jurkat cell line exposed to doxorubicin

Żuryń, Agnieszka; Litwiniec, Anna; Gackowska, Lidia; Pawlik, Andrzej; Grzanka, Alina

doi:10.1042/cbi20120274

Cited by 22 publications

(7 citation statements)

References 35 publications

(38 reference statements)

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“…Therefore, it would be tempting to hypothesize that increased levels of cyclin D1 may somehow reflect or even promote these cells to enter the S phase and proliferate further, especially as we have shown in our cyclin D1/PI double staining experiment that the highest levels of cyclin D1 are indicative of G2/M population and particularly of the fraction of polyploid cells. In previous studies we also found that the levels/fluorescence of cyclin D1 increased in the G2/M and polyploidy after treatment with doxorubicin in the Jurkat and A549 cell lines (Żuryń et al, ; Litwiniec et al, ). The percentage of subG 1 fraction as well as early and late apoptotic cells, as evidenced by annexin V/PI staining, is visibly increased starting from this concentration and the number of G0/G1‐cyclin D1‐positive cells decreased, whereas the respective values were also reduced in the S‐ and G2/M‐phases with 0.3 µM doxorubicin, which suggests that induction of cell death pathways most probably contribute to observed reductions in the number of polyploid cells.…”

Section: Discussionsupporting

confidence: 52%

Expression of cyclin D1 after treatment with doxorubicin in the HL‐60 cell line

Żuryń

Litwiniec

Klimaszewska‐Wiśniewska

et al. 2014

Cell Biology International

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Increased levels of cyclin D1 and amplification of CCND1 gene occur in many types of cancers. We have followed the expression of cyclin D1 after treatment with doxorubicin with reference to cell death and other possible therapeutic implications. The effect of the treatment on the cell cycle, survival, intracellular level (flow cytometry), and intracellular localization of cyclin D1 (fluorescence microscopy) and expression of CCND1 (real-time RT-PCR) was investigated in HL-60 cells. An increase in the fluorescence intensity of cyclin D1 occurred after treatment with 0.15 and 0.3 μM doxorubicin. This tendency was confirmed by real-time RT-PCR. Expression of CCND1 in relation to the reference gene PBGD was increased in cells exposed to 0.15 μM doxorubicin. Concomitantly, some alterations in the regulation of the G0/G1, S, and G2/M checkpoints occurred, accompanied by changes in the polyploid fraction of the population. This was particularly evident at 0.3 μM doxorubicin, at which concentration the rate of cell death was also clearly higher. In conclusion, depending on the concentration used, alterations in cell death and the number of S, G2/M, and polyploid cells may correspond with cyclin D1 levels. This, in turn, may reflect an important role of the protein as one of the possible survival/point-of-no-return regulators dependent on its concentration, which seems especially plausible in the context of more prominent cell death in the above-mentioned fractions of cells.

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Section: Discussionsupporting

confidence: 52%

Expression of cyclin D1 after treatment with doxorubicin in the HL‐60 cell line

Żuryń

Litwiniec

Klimaszewska‐Wiśniewska

et al. 2014

Cell Biology International

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“…Cyclin D1 plays a crucial role in tumorigenesis, which propels cell cycle progression at the G1/S stage and promotes the proliferation of cancer cells [18,19]. As a result, it is also recommended as an important biomarker of pathological diagnosis and therapy for different cancers [20,21].…”

Section: Discussionmentioning

confidence: 99%

SDF-1/CXCR4 signaling up-regulates survivin to regulate human sacral chondrosarcoma cell cycle and epithelial–mesenchymal transition via ERK and PI3K/AKT pathway

et al. 2014

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Human sacral chondrosarcoma, the most common one of malignant tumors, has a potent capacity to invade locally and metastasize. Notably, CXCR4 and survivin are widely recommended as a candidate of the molecule-targeted therapy. However, the roles and associations of CXCR4 and survivin in sacral chondrosarcoma have not been well characterized. Here, we investigated CXCR4 and survivin expression in human sacral chondrosarcoma. Resected sacral chondrosarcoma specimens were available from 30 patients. In vitro human chondrosarcoma cell lines SW1353 was used. Immunohistochemistry, Western blot, RNA interference, and cell cycle analyses were conducted. Immunohistochemistry revealed that CXCR4 and survivin expressed in 83.3 and 86.7 % of sacral chondrosarcoma tissues, respectively, and both were closely associated with grade and recurrence (p < 0.05). Western blot revealed that survivin expression in SW1353 increased in a dose- and time-dependent manner following SDF-1 treatment. However, the interference with MEK/ERK and PI3K/AKT pathway affected SDF-1-induced up-regulation of survivin. Besides survivin siRNA affected cell cycle progression and the expression of epithelial-mesenchymal transition (EMT) biomarkers: Snail and N-cadherin, when compared with those of non-transfection. In conclusion, the present study shows that SDF-1/CXCR4 signaling up-regulates survivin via MEK/ERK and PI3K/AKT pathway, leading to cell cycle and EMT occurrence in human sacral chondrosarcoma. The antagonizing of CXCR4 and/or survivin might benefit patients with sacral chondrosarcoma.

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“…In previous studies, different levels of doxorubicin dose produced different cell death pathways, and lower doses may induce G2/M arrest (28,29). To investigate whether fulvestrant also enhanced doxorubicin-induced G2/M arrest, cell cycle distribution was analysed by flow cytometric assay (Fig.…”

Section: Resultsmentioning

confidence: 93%

Fulvestrant reverses doxorubicin resistance in multidrug-resistant breast cell lines independent of estrogen receptor expression

et al. 2016

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Drug resistance, a major obstacle to successful cancer chemotherapy, frequently occurs in recurrent or metastatic breast cancer and results in poor clinical response. Fulvestrant is a new type of selective estrogen receptor (ER) downregulator and a promising endocrine therapy for breast cancer. In this study, we evaluated the combination treatment of fulvestrant and doxorubicin in ER-negative multidrug-resistant (MDR) breast cancer cell lines Bads-200 and Bats-72. Fulvestrant potentiated doxorubicin-induced cytotoxicity, apoptosis and G2/M arrest with upregulation of cyclin B1. It functioned as a substrate for P-glycoprotein (P-gp) without affecting its expression. Furthermore, fulvestrant not only restored the intracellular accumulation of doxorubicin but also relocalized it to the nuclei in Bats-72 and Bads-200 cells, which may be another potential mechanism of reversal of P-gp mediated doxorubicin resistance. These results indicated that the combination of fulvestrant and doxorubicin-based chemotherapy may be feasible and effective for patients with advanced breast cancer.

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Expression of cyclin A, B1 and D1 after induction of cell cycle arrest in the Jurkat cell line exposed to doxorubicin

Cited by 22 publications

References 35 publications

Expression of cyclin D1 after treatment with doxorubicin in the HL‐60 cell line

Expression of cyclin D1 after treatment with doxorubicin in the HL‐60 cell line

SDF-1/CXCR4 signaling up-regulates survivin to regulate human sacral chondrosarcoma cell cycle and epithelial–mesenchymal transition via ERK and PI3K/AKT pathway

Fulvestrant reverses doxorubicin resistance in multidrug-resistant breast cell lines independent of estrogen receptor expression

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