Suppression of SCIN inhibits human prostate cancer cell proliferation and induces G0/G1 phase arrest

Wang, Dong; Sun, Shu-Qing; Yu, Yinhua; Wu, Wei; Yang, Shaodong; Tan, Jianming

doi:10.3892/ijo.2013.2170

Cited by 55 publications

(52 citation statements)

References 22 publications

(23 reference statements)

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“…Previous studies suggest that Mith inhibits growth of human cancers by decreasing Sp1 protein232425, but how Sp1 protein is decreased by Mith is not clear. We checked Sp1 mRNA levels in cervical cancer cell lines and saw no significant difference in cells with or without Mith treatment (Fig.…”

Section: Resultsmentioning

confidence: 98%

“…Previous studies have suggested that Mith inhibits the growth of various human cancers by decreasing Sp1 protein level232425, but it is still not clear how Sp1 protein level is decreased by Mith. We first checked the mRNA expression levels of Sp1 in different cervical cancer cell lines.…”

Section: Resultsmentioning

confidence: 99%

“…Both stability and transcriptional activity contribute to enhanced Sp1 protein levels observed during tumorigenesis35. Previous studies suggest that Mith inhibits the growth of various human cancers by decreasing Sp1 protein232425, but how Sp1 protein is decreased by Mith is unclear. Many transcription factors can be degraded by the proteasome36.…”

Section: Discussionmentioning

confidence: 99%

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Modulation of specificity protein 1 by mithramycin A as a novel therapeutic strategy for cervical cancer

Choi

Nam

Jung

et al. 2014

Sci Rep

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Cervical cancer is the third most common cancer and the third leading cause of death among women. However, the standard treatment for cervical cancer includes cisplatin, which can cause side effects such as hematological damage or renal toxicity. New innovations in cervical cancer treatment focus on developing more effective and better-tolerated therapies such as Sp1-targeting drugs. Previous studies suggested that mithramycin A (Mith) inhibits the growth of various cancers by decreasing Sp1 protein. However, how Sp1 protein is decreased by Mith is not clear. Few studies have investigated the regulation of Sp1 protein by proteasome-dependent degradation as a possible control mechanism for the regulation of Sp1 in cancer cells. Here, we show that Mith decreased Sp1 protein by inducing proteasome-dependent degradation, thereby suppressing cervical cancer growth through a DR5/caspase-8/Bid signaling pathway. We found that prolonged Mith treatment was well tolerated after systemic administration to mice carrying cervical cancer cells. Reduction of body weight was minimal, indicating that Mith was a good therapeutic candidate for treatment of cancers in which Sp1 is involved in promoting and developing disease.

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Section: Resultsmentioning

confidence: 98%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Modulation of specificity protein 1 by mithramycin A as a novel therapeutic strategy for cervical cancer

Choi

Nam

Jung

et al. 2014

Sci Rep

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“…After 1, 2, 3, 4, and 5 days of incubation, viable cells were analyzed using MTT plus acidic isopropanol (10% SDS, 5% isopropanol, and 0.01 M HCl), as described in a previous report. 19 The absorbance of each well was recorded at the wavelength of 595 nm using a microplate reader. Experiments were performed in triplicate.…”

Section: Mtt Assaymentioning

confidence: 99%

Downregulation ofSKA1Gene Expression Inhibits Cell Growth in Human Bladder Cancer

Tian

Xing

et al. 2015

Cancer Biotherapy and Radiopharmaceuticals

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Spindle and kinetochore-associated protein 1 (SKA1), a component of microtubule-binding complex of kinetochore, is essential for proper chromosome segregation. Recently, SKA1 has been shown to be involved in malignant progression of several human cancers. However, its role in bladder cancer is still unknown. To evaluate the function of SKA1 in bladder cancer cells, the authors employed an RNA interference lentivirus system to deplete its expression in both BT5637 and T-24 bladder cancer cells. The cell proliferation was significantly decreased in both cell lines after SKA1 knockdown. Moreover, the colony formation capacity was impaired by SKA1 silencing. Flow cytometry analysis showed that depletion of SKA1 led to cell cycle arrest at S phase. Furthermore, knockdown of SKA1 in T-24 cells obviously downregulated the expressions of CDK4 and Cyclin D1, and alleviated the activations of ERK2 and AKT, conducive to cell growth inhibition. These findings suggested that knockdown of SKA1 could potently suppress bladder cancer cell proliferation in vitro and lentivirus-mediated silencing of SKA1 might serve as a novel strategy for gene therapy of bladder cancer.

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“…79, 80, 83–85 For example, higher stage gliomas have been found to over-express DNA damage tolerance components. 86 Over-expression of hpol κ was observed in 23 out of 40 glioma patients (57.5%) and hpol ι in 11 of 40 (27.5%), while there was no observable change in hpol η expression between glioma patients and normal tissue.…”

Section: Mis-regulation Of Tls Occurs In Cancer Is Related To Diseasmentioning

confidence: 99%

Aberrant Kynurenine Signaling Modulates DNA Replication Stress Factors and Promotes Genomic Instability in Gliomas

Bostian

Eoff

2016

Chem. Res. Toxicol.

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Metabolism of the essential amino acid L-tryptophan (TRP) is implicated in a number of neurological conditions including depression, neurodegenerative diseases, and cancer. The TRP catabolite kynurenine (KYN) has recently emerged as an important neuroactive factor in brain tumor pathogenesis, with additional studies implicating KYN in other types of cancer. Often highlighted as a modulator of the immune response and a contributor to immune escape for malignant tumors, it is well known that KYN has effects on the production of the co-enzyme nicotinamide adenine dinucleotide (NAD+), which can have a direct impact on DNA repair, replication, cell division, redox signaling, and mitochondrial function. Additional effects of KYN signaling are imparted through its role as an endogenous agonist for the aryl hydrocarbon receptor (AhR), and it is largely through activation of the AhR that KYN appears to mediate malignant progression in gliomas. We have recently reported on the ability of KYN signaling to modulate expression of human DNA polymerase kappa (hpol κ), a translesion enzyme involved in bypass of bulky DNA lesions and activation of the replication stress response. Given the impact of KYN on NAD+ production, AhR signaling, and translesion DNA synthesis, it follows that dysregulation of KYN signaling in cancer may promote malignancy through alterations in the level of endogenous DNA damage and replication stress. In the following perspectives article, we discuss the connections between KYN signaling, DNA damage tolerance, and genomic instability, as they relate to cancer.

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Suppression of SCIN inhibits human prostate cancer cell proliferation and induces G0/G1 phase arrest

Cited by 55 publications

References 22 publications

Modulation of specificity protein 1 by mithramycin A as a novel therapeutic strategy for cervical cancer

Modulation of specificity protein 1 by mithramycin A as a novel therapeutic strategy for cervical cancer

Downregulation ofSKA1Gene Expression Inhibits Cell Growth in Human Bladder Cancer

Aberrant Kynurenine Signaling Modulates DNA Replication Stress Factors and Promotes Genomic Instability in Gliomas

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