Exploring the roles of basal transcription factor 3 in eukaryotic growth and development

Jamil, Muhammad; Wang, Wenyi; Xu, Mengyun; Tu, J. C.

doi:10.1080/02648725.2015.1080064

Cited by 14 publications

(7 citation statements)

References 98 publications

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“…Curiously, at 48 h post transfection the secreted protein levels decreased drastically regardless of changes in mRNA levels prior to this timepoint. Basal transcription factor 3 (BTF3) has been reported to play a significant role in the transcriptional regulation related to eukaryote growth and development [ 89 ]. In LL5 cells it showed increased mRNA levels at 12 h and increased secreted protein level 12 h after mRNA increase.…”

Section: Resultsmentioning

confidence: 99%

Identification of Secreted Proteins Involved in Nonspecific dsRNA-Mediated Lutzomyia longipalpis LL5 Cell Antiviral Response

Martins-da-Silva

Telleria

Batista

et al. 2018

Viruses

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Hematophagous insects transmit infectious diseases. Sand flies are vectors of leishmaniasis, but can also transmit viruses. We have been studying immune responses of Lutzomyia longipalpis, the main vector of visceral leishmaniasis in the Americas. We identified a non-specific antiviral response in L. longipalpis LL5 embryonic cells when treated with non-specific double-stranded RNAs (dsRNAs). This response is reminiscent of interferon response in mammals. We are investigating putative effectors for this antiviral response. Secreted molecules have been implicated in immune responses, including interferon-related responses. We conducted a mass spectrometry analysis of conditioned medium from LL5 cells 24 and 48 h after dsRNA or mock treatment. We identified 304 proteins. At 24 h, 19 proteins had an abundance equal or greater than 2-fold change, while the levels of 17 proteins were reduced when compared to control cells. At the 48 h time point, these numbers were 33 and 71, respectively. The two most abundant secreted peptides at 24 h in the dsRNA-transfected group were phospholipid scramblase, an interferon-inducible protein that mediates antiviral activity, and forskolin-binding protein (FKBP), a member of the immunophilin family, which mediates the effect of immunosuppressive drugs. The transcription profile of most candidates did not follow the pattern of secreted protein abundance.

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Section: Resultsmentioning

confidence: 99%

Identification of Secreted Proteins Involved in Nonspecific dsRNA-Mediated Lutzomyia longipalpis LL5 Cell Antiviral Response

Martins-da-Silva

Telleria

Batista

et al. 2018

Viruses

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“…It is believed that BTF3 is intimately involved in the regulation of a number of biological processes. 11 Its interaction with promoter elements, such as CAAT and TATA box sequences, initiates polymerase transcription by RNA. In addition, previous research has confirmed that BTF3 regulates regulation of the cell cycle as well as apoptosis.…”

Section: Discussionmentioning

confidence: 99%

BTF3 Silencing Inhibits the Proliferation of Osteosarcoma Cells

et al. 2019

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Osteosarcoma (OS) is one of the bone malignancy cancers with poor prognosis in the early stages worldwide. Basic transcription factor 3 (BTF3) is associated with the development of several types of cancer. The present study aimed to evaluate the role of BTF3 in OS. Silencing of BTF3 was achieved by using stable lentivirus transfection of siRNA targeting BTF3 in the human OS cell line Saos-2. Cell viability and colony-forming ability were measured using methyl-thaizolyl-tetrazolium (MTT) and colony formation assays, respectively. Propidium iodide staining and flow cytometry was used to detect the progression of the cell cycle. To evaluate the possible intracellular signaling molecules involved, a PathScan Intracellular Signaling Array Kit was utilized. Lentivirus-BTF3-shRNA (LV-BTF3-shRNA) suppressed expression of BTF3 in Saos-2 cells (inhibition ratio: 89.8%), which significantly inhibited cell proliferation (48.5%), colony formation and enhanced apoptosis to 48.2% compared to 4.5% with lentivirus control shRNA (N-shRNA). Additionally, BTF3 silencing enhanced the percentage of Saos-2 cells in S and G 2 /M phases, but significantly reduced cells in the G0/M phase (all P < 0.01). The proteins activated by BTF3 included STAT3, S6 ribosomal protein, HSP27 and SAPK/JNK2, all of which were inhibited by BTF3 silencing, whereas SAPK/JNK1 was upregulated by BTF3 silencing. In the present study, we explored the crucial role of BTF3 in promoting OS cell proliferation as well as laying the foundations for further research to investigate the clinical potential of lentivirus-mediated delivery of BTF3 interruption therapy for the treatment of OS.

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“…We next generated PC-3 and DU145 cells stably overexpressing one of the two BTF3 splicing isoforms, BTF3a or BTF3b 17,18 , and subjected them for further functional characterization. Indeed, ectopic overexpression of either BTF3 isoform resulted in markedly enhanced cell growth (Fig.…”

Section: Btf3b Exerts Its Oncogenic Effects Through Transcriptional Rmentioning

confidence: 99%

“…Basic transcription factor 3 (BTF3), also known as the beta subunit of the nascent polypeptide-associated complex, was originally reported to be a member of general transcription machinery and form a stable complex with the RNA polymerase II to initiate transcription 16,17 . BTF3 exists in two splicing isoforms, BTF3a and BTF3b.…”

Section: Introductionmentioning

confidence: 99%

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BTF3 confers oncogenic activity in prostate cancer through transcriptional upregulation of Replication Factor C

Zhang

Gao

et al. 2021

Cell Death Dis

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High levels of Basic Transcription Factor 3 (BTF3) have been associated with prostate cancer. However, the mechanisms underlying the role of BTF3 as an oncogenic transcription factor in prostate tumorigenesis have not been explored. Herein, we report that BTF3 confers oncogenic activity in prostate cancer cells. Mechanistically, while both BTF3 splicing isoforms (BTF3a and BTF3b) promote cell growth, BTF3b, but not BTF3a, regulates the transcriptional expression of the genes encoding the subunits of Replication Factor C (RFC) family that is involved in DNA replication and damage repair processes. BTF3 knockdown results in decreased expression of RFC genes, and consequently attenuated DNA replication, deficient DNA damage repair, and increased G2/M arrest. Furthermore, knockdown of the RFC3 subunit diminishes the growth advantage and DNA damage repair capability conferred by ectopic overexpression of BTF3b. Importantly, we show that enforced BTF3 overexpression in prostate cancer cells induces substantial accumulation of cisplatin-DNA adducts and render the cells more sensitive to cisplatin treatment both in vitro and in vivo. These findings provide novel insights into the role of BTF3 as an oncogenic transcription factor in prostate cancer and suggest that BTF3 expression levels may serve as a potential biomarker to predict cisplatin treatment response.

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Exploring the roles of basal transcription factor 3 in eukaryotic growth and development

Cited by 14 publications

References 98 publications

Identification of Secreted Proteins Involved in Nonspecific dsRNA-Mediated Lutzomyia longipalpis LL5 Cell Antiviral Response

Identification of Secreted Proteins Involved in Nonspecific dsRNA-Mediated Lutzomyia longipalpis LL5 Cell Antiviral Response

BTF3 Silencing Inhibits the Proliferation of Osteosarcoma Cells

BTF3 confers oncogenic activity in prostate cancer through transcriptional upregulation of Replication Factor C

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