Knockdown of cullin 4A inhibits growth and increases chemosensitivity in lung cancer cells

Hung, Ming‐Szu; Chen, I‐Chuan; Li, You; Jablons, David M.; Li, Ya‐Chin; Mao, Jian‐Hua; Xu, Zhidong; Lung, Jrhau; Yang, Cheng‐Ta; Liu, Shih‐Tung

doi:10.1111/jcmm.12811

Cited by 13 publications

(14 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…RNA concentration and integrity were determined by measuring the absorbance at 260 nm. The cDNA was performed using 5 μg of total RNA, 200 U of Superscript III, and 0.5 μg of oligo dT (12)(13)(14)(15)(16)(17)(18) under the following conditions: 42˚C for 90 min, followed by heating at 70˚C for 10 min. The cDNA obtained was amplified using Taq DNA polymerase (Life Technologies) and Wt1 primers: 5'-AACGCCCCTTCATGTGTGC-3' and 5'-GCTGGTCTGAACGAGAAAACCTTC-3' to amplify a fragment of 150 bp.…”

Section: Methodsmentioning

confidence: 99%

“…For this reason, WT1 is considered a good target for anticancer therapy (12). The silencing of genes involved in proliferation and apoptosis are an attractive strategy for the development of anticancer therapies (13)(14)(15), and for sensitizing tumor cells to chemotherapy (14). It has been observed that silencing genes such as B-cell lymphoma 2 (BCL2) and BCL-xL sensitizes cisplatin-resistant cells (16,17).…”

mentioning

confidence: 99%

See 1 more Smart Citation

shRNA-WT1 Potentiates Anticancer Effects of Gemcitabine and Cisplatin Against B16F10 Lung MetastasesIn VitroandIn Vivo

Zapata‐Benavides¹,

Thompson-Armendariz²,

Arellano-Rodríguez³

et al. 2019

In Vivo

View full text Add to dashboard Cite

Background/Aim: High expression level of Wilm's tumor gene (WT1) in several types of tumors appears to confer disruption of apoptosis and resistance to chemotherapeutic drugs, and correlate with poor outcome. The aim of this work was to determine if down-regulation of WT1 expression results in decreased cell proliferation and the increased action of different types of drugs, both in vitro in B16F10 cells, and in vivo in C57BL/6 mice. Materials and Methods: Inhibition of cell proliferation by short hairpin RNA against WT1 (shRNA-WT1), cisplatin, and gemcitabine in B16F10 cells in vitro was determined by the MTT assay and analysis of clonogenic survival. The apoptosis rate was determined by flow cytometry for annexin-V-fluorescein isothiocyante and propidium iodide. Results: Compared to treatment with shRNA-WT1 alone, treatment with shRNA-WT1 in combination with drugs had a synergistic inhibitory effect on B16F10 cell proliferation, particularly for the combination of cisplatin and gemcitabine at their 25% cytotoxic concentrations in vitro. Furthermore, mice treated with shRNA-WT1 in combination with cisplatin and gemcitabine were protected in the same way as those treated with the drugs alone, but were in better physical condition. Conclusion: Decreased WT1 expression induces cell death and potentiates the action of anticancer drugs by inducing synergistic effects both in vitro and in vivo, which may be an attractive strategy in lung cancer therapy.

show abstract

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

shRNA-WT1 Potentiates Anticancer Effects of Gemcitabine and Cisplatin Against B16F10 Lung MetastasesIn VitroandIn Vivo

Zapata‐Benavides¹,

Thompson-Armendariz²,

Arellano-Rodríguez³

et al. 2019

In Vivo

View full text Add to dashboard Cite

show abstract

“…Furthermore, in vitro and in vivo studies showed decreased tumor growth and increased chemo-sensitivity to gemcitabine through G0/G1 cell cycle arrest after Cul4A (cullin 4A) knockdown, which is an important regulator of proliferation and cell cycle progression in lung cancer. In addition, Cul4A knockdown increases the expression of KLF10, cyclin-dependent kinase inhibitor p21/WAF1, and TGF-β1, which play a role as tumor suppressors [ 92 ].…”

Section: Role Of Klf10 As a Tumor Suppressor In Various Cancersmentioning

confidence: 99%

KLF10 as a Tumor Suppressor Gene and Its TGF-β Signaling

Memon

Lee

2018

Cancers

View full text Add to dashboard Cite

Krüppel-like factor 10 (KLF10), originally named TGF-β (Transforming growth factor beta) inducible early gene 1 (TIEG1), is a DNA-binding transcriptional regulator containing a triple C2H2 zinc finger domain. By binding to Sp1 (specificity protein 1) sites on the DNA and interactions with other regulatory transcription factors, KLF10 encourages and suppresses the expression of multiple genes in many cell types. Many studies have investigated its signaling cascade, but other than the TGF-β/Smad signaling pathway, these are still not clear. KLF10 plays a role in proliferation, differentiation as well as apoptosis, just like other members of the SP (specificity proteins)/KLF (Krüppel-like Factors). Recently, several studies reported that KLF10 KO (Knock out) is associated with defects in cell and organs such as osteopenia, abnormal tendon or cardiac hypertrophy. Since KLF10 was first discovered, several studies have defined its role in cancer as a tumor suppressor. KLF10 demonstrate anti-proliferative effects and induce apoptosis in various carcinoma cells including pancreatic cancer, leukemia, and osteoporosis. Collectively, these data indicate that KLF10 plays a significant role in various biological processes and diseases, but its role in cancer is still unclear. Therefore, this review was conducted to describe and discuss the role and function of KLF10 in diseases, including cancer, with a special emphasis on its signaling with TGF-β.

show abstract

“…In esophageal cancer, secreted-TGFBI has been detected in the ECM and tumor vasculature by immunohistochemistry [ 37 ]. TGFBI expression is regulated not only by TGF-β, but also by other mechanisms including autophagy [ 38 , 39 ], microRNAs [ 40 ], retinoid [ 41 ], interleukin (IL)-1β, tumor necrosis factor-α [ 42 ], IL-4 [ 43 ], secreted protein acidic and rich in cysteine [ 44 ], 4-phenylbutyric acid [ 45 ], and cullin 4A [ 46 ] ( Figure 1 ). The mechanism of TGFBI regulation merits more detailed investigation as a potential therapeutic target.…”

Section: Role Of Tgf-β In Cancermentioning

confidence: 99%

TGF-β Signaling in Gastrointestinal Cancers: Progress in Basic and Clinical Research

Yokobori

Nishiyama

2017

JCM

View full text Add to dashboard Cite

Transforming growth factor (TGF)-β superfamily proteins have many important biological functions, including regulation of tissue differentiation, cell proliferation, and migration in both normal and cancer cells. Many studies have reported that TGF-β signaling is associated with disease progression and therapeutic resistance in several cancers. Similarly, TGF-β-induced protein (TGFBI)—a downstream component of the TGF-β signaling pathway—has been shown to promote and/or inhibit cancer. Here, we review the state of basic and clinical research on the roles of TGF-β and TGFBI in gastrointestinal cancers.

show abstract

Knockdown of cullin 4A inhibits growth and increases chemosensitivity in lung cancer cells

Cited by 13 publications

References 38 publications

shRNA-WT1 Potentiates Anticancer Effects of Gemcitabine and Cisplatin Against B16F10 Lung MetastasesIn VitroandIn Vivo

shRNA-WT1 Potentiates Anticancer Effects of Gemcitabine and Cisplatin Against B16F10 Lung MetastasesIn VitroandIn Vivo

KLF10 as a Tumor Suppressor Gene and Its TGF-β Signaling

TGF-β Signaling in Gastrointestinal Cancers: Progress in Basic and Clinical Research

Contact Info

Product

Resources

About