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Role of CTCF poly(ADP-Ribosyl)ation in the regulation of apoptosis in breast cancer cells.

Venkatraman B, Klenova E - Indian J Med Paediatr Oncol (2015 Jan-Mar)

Bottom Line: CTCF is a candidate tumor suppressor gene encoding a multifunctional transcription factor.CTCF function is controlled by posttranslational modification and interaction with other proteins.The effect of CTCF-WT and CTCF complete mutant was expressed in breast cancer cell-lines by DNA-mediated transfection technique monitored by enhanced green fluorescent protein fluorescence.

View Article: PubMed Central - PubMed

Affiliation: Australian School of Advanced Medicine, Macquarie University, Sydney, Australia.

ABSTRACT

Introduction: CTCF is a candidate tumor suppressor gene encoding a multifunctional transcription factor. CTCF function is controlled by posttranslational modification and interaction with other proteins. Research findings suggested that CTCF function can be regulated by poly(ADP-ribosyl)ation (PARlation) and has specific anti-apoptotic function in breast cancer cells. The aim of this study is to assess the effect of CTCF-wild type (WT) and CTCF complete mutant, which is deficient of PARlation in regulating apoptosis in breast cancer cells.

Materials and methods: The effect of CTCF-WT and CTCF complete mutant was expressed in breast cancer cell-lines by DNA-mediated transfection technique monitored by enhanced green fluorescent protein fluorescence. Evaluation of apoptotic cell death was carried out with immunohistochemical staining using 4'-6'-diamino-2 phenylindole and scoring by fluorescent microscopy.

Results: CTCF-WT supports survival of breast cancer cells and was observed that CTCF complete mutant interferes with the functions of the CTCF-WT and there was a considerable apoptotic cell death in the breast cancer cell lines such as MDA-MB-435, CAMA-1 and MCF-7.

Conclusion: The study enlighten CTCF as a Biological Marker for breast cancer and the role of CTCF PARlation may be involved in breast carcinogenesis.

No MeSH data available.


Related in: MedlinePlus

Bar graph shows the percent apoptosis on the sodium butyrate treated and transfected MDA-MB-435 cell line. The percent efficiency has been recorded as 51% at 24 h and 73% at 48 h
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Figure 4: Bar graph shows the percent apoptosis on the sodium butyrate treated and transfected MDA-MB-435 cell line. The percent efficiency has been recorded as 51% at 24 h and 73% at 48 h

Mentions: Finally, studies on the effect of transfection and NaB have been carried out on the above mentioned breast cancer cell lines such as CAMA-1, MCF-7 and MDA-MB-435. The results have been tabulated. From the readings it was observed that the efficiency of transfection on NaB treated complete mutant 4 MDA-MB-435 cell line showed the maximum at 48 h as 77% [Table 1], followed by CAMA-1 [Table 2] showing 56% and MCF-7 with 30% at 48 h, respectively [Table 3]. The results were also recorded for the apoptosis on all the above mentioned transfected and NaB treated cell lines using BX41 Fluorescent Microscopy. The highest recorded apoptotic cell death was observed in MDA-MB-435 cell line showing 51% at 24 h and 73% in 48 h with complete mutant 4 [Figure 4] in comparison to that of CAMA-1 [Figure 5] and MCF-7 [Figure 6].


Role of CTCF poly(ADP-Ribosyl)ation in the regulation of apoptosis in breast cancer cells.

Venkatraman B, Klenova E - Indian J Med Paediatr Oncol (2015 Jan-Mar)

Bar graph shows the percent apoptosis on the sodium butyrate treated and transfected MDA-MB-435 cell line. The percent efficiency has been recorded as 51% at 24 h and 73% at 48 h
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4363851&req=5

Figure 4: Bar graph shows the percent apoptosis on the sodium butyrate treated and transfected MDA-MB-435 cell line. The percent efficiency has been recorded as 51% at 24 h and 73% at 48 h
Mentions: Finally, studies on the effect of transfection and NaB have been carried out on the above mentioned breast cancer cell lines such as CAMA-1, MCF-7 and MDA-MB-435. The results have been tabulated. From the readings it was observed that the efficiency of transfection on NaB treated complete mutant 4 MDA-MB-435 cell line showed the maximum at 48 h as 77% [Table 1], followed by CAMA-1 [Table 2] showing 56% and MCF-7 with 30% at 48 h, respectively [Table 3]. The results were also recorded for the apoptosis on all the above mentioned transfected and NaB treated cell lines using BX41 Fluorescent Microscopy. The highest recorded apoptotic cell death was observed in MDA-MB-435 cell line showing 51% at 24 h and 73% in 48 h with complete mutant 4 [Figure 4] in comparison to that of CAMA-1 [Figure 5] and MCF-7 [Figure 6].

Bottom Line: CTCF is a candidate tumor suppressor gene encoding a multifunctional transcription factor.CTCF function is controlled by posttranslational modification and interaction with other proteins.The effect of CTCF-WT and CTCF complete mutant was expressed in breast cancer cell-lines by DNA-mediated transfection technique monitored by enhanced green fluorescent protein fluorescence.

View Article: PubMed Central - PubMed

Affiliation: Australian School of Advanced Medicine, Macquarie University, Sydney, Australia.

ABSTRACT

Introduction: CTCF is a candidate tumor suppressor gene encoding a multifunctional transcription factor. CTCF function is controlled by posttranslational modification and interaction with other proteins. Research findings suggested that CTCF function can be regulated by poly(ADP-ribosyl)ation (PARlation) and has specific anti-apoptotic function in breast cancer cells. The aim of this study is to assess the effect of CTCF-wild type (WT) and CTCF complete mutant, which is deficient of PARlation in regulating apoptosis in breast cancer cells.

Materials and methods: The effect of CTCF-WT and CTCF complete mutant was expressed in breast cancer cell-lines by DNA-mediated transfection technique monitored by enhanced green fluorescent protein fluorescence. Evaluation of apoptotic cell death was carried out with immunohistochemical staining using 4'-6'-diamino-2 phenylindole and scoring by fluorescent microscopy.

Results: CTCF-WT supports survival of breast cancer cells and was observed that CTCF complete mutant interferes with the functions of the CTCF-WT and there was a considerable apoptotic cell death in the breast cancer cell lines such as MDA-MB-435, CAMA-1 and MCF-7.

Conclusion: The study enlighten CTCF as a Biological Marker for breast cancer and the role of CTCF PARlation may be involved in breast carcinogenesis.

No MeSH data available.


Related in: MedlinePlus