High Levels of KAP1 Expression Are Associated with Aggressive Clinical Features in Ovarian Cancer

Cui, Yanfen; Yang, Shaobin; Fu, Xin; Feng, Jingwen; Xu, Shilei; Ying, Guoguang

doi:10.3390/ijms16010363

Cited by 46 publications

(45 citation statements)

References 26 publications

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“…20 μg of protein was separated on a 10% of SDS-PAGE gel and blotted onto a PVDF membrane. 5% of fat-free milk blocks the membrane, which was then incubated with primary antibody for 1h and secondary antibody for 1h at room temperature [31]. The antibodies used in this study as following: FAS (Santa Cruz, Cat#sc-48357), Bcl-2 (Abcam, Cat#ab692), Bcl-xL (Abcam, Cat#ab77571).…”

Section: Methodsmentioning

confidence: 99%

NADPH accumulation is responsible for apoptosis in breast cancer cells induced by fatty acid synthase inhibition

et al. 2017

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Fatty acid synthase (FAS), as a key enzyme involved in de novo lipogenesis, is highly expressed in many cancers. FAS inhibition induces cell death in vivo and in vitro, rendering FAS as an attractive target for cancer therapy, but the defined mechanism is still not well understood. Herein, we confirmed that FAS was highly expressed in breast cancers and FAS inhibition by its inhibitors or knockdown induced apoptosis in breast cancer cells. Our results showed that a significantly high level of reactive oxygen species was induced but not responsible for apoptosis in breast cancer cells by FAS inhibition. Instead, NADPH accumulation resulting from FAS inhibition was found to stimulate NADPH oxidase to generate reactive oxygen species and highly associated with apoptosis induction. Suppression of NADPH oxidase almost totally blocked reactive oxygen species generation while significantly potentiated the in vitro and in vivo killing of breast cancers by FAS inhibition. Taken together, these data suggest that FAS plays a critical role in maintaining cellular redox homeostasis and its inhibition leads to NADPH accumulation-mediated apoptosis. Our finding may provide new insights into cancer metabolism and aid in designing effective anticancer treatments.

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Section: Methodsmentioning

confidence: 99%

NADPH accumulation is responsible for apoptosis in breast cancer cells induced by fatty acid synthase inhibition

et al. 2017

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“…In one animal model, 2⨰10 6 OVCAR8 cells were injected subcutaneously to the dorsal midline in 10 nu/nu mice to generate murine subcutaneous tumors. When the tumor size reached the size of approximately 60-80 mm 3 , these mice were divided into two groups randomly: control group (water without fructose, n=5), fructose-feeding group (water with 15% fructose, n=5), and the standard laboratory chow was given to all the mice. In the second model, 2⨰10 6 OVCAR8 of sgctrl, sgGLUT5#1, and sgGLUT5#1-GLUT5 cells were injected subcutaneously to the dorsal midline in nu/nu 15 mice, followed by 15% fructose water feeding and standard laboratory chow.…”

Section: Mice Xenograft Modelsmentioning

confidence: 99%

“…However, since cancer of the ovary is located deep within the pelvis and difficult to assess, and has no early typical symptoms and effective diagnostic methods, 65-75% women with cancer of the ovary are frequently diagnosed with advanced stage disease. [1][2][3] So cancer of the ovary has the highest case fatality rate, accounting for almost half of the deaths from gynecologic malignancies. 4 After years of study, researchers have discovered several risk factors that might increase a woman's chance of developing ovarian cancer, among them, obesity is the most important risk factor.…”

Section: Introductionmentioning

confidence: 99%

<p>GLUT5 increases fructose utilization in ovarian cancer</p>

Jin¹,

Gong²,

Shang³

2019

OTT

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Background: Fructose is one of the most common dietary carbohydrates in the whole world, and recent studies have found that fructose consumption is closely related to the oncogenesis and development of tumors, however, very few studies have focused on the fructose in ovarian cancer. GLUT5 (Glucose transporter type 5), as a specific fructose transporter in mammalian cells, has also been found highly expressed in many cancers. Methods: In this study, we investigated the abilities of proliferation, colony formation, and migration of ovarian cancer cells in fructose medium, and then silenced GLUT5 in ovarian cancer cells to explore the role GLUT5 in fructose metabolism in ovarian cancer. Results: The results showed that the ovarian cancer cells had similar abilities of proliferation and migration in fructose medium and glucose medium, but silencing GLUT5 could significantly inhibit these abilities in fructose medium. Meanwhile, we found that GLUT5 was higher expressed in ovarian cancer tissues, and its expression correlated significantly with tumor malignancy and poor survival of ovarian cancer patients. Furthermore, the results of animal experiments also demonstrated that intake too much fructose could prominently increase tumor volume, and silencing GLUT5 could significantly inhibit tumor proliferation. Conclusion: In conclusion, we demonstrate that ovarian cancer cells could utilize fructose for their growth, and restricting the fructose intake or targeting GLUT5 may be efficacious strategies for ovarian cancer therapy.

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“…Several studies demonstrated that TRIM28 overexpression was always associated with clinicopathological features, which gives prominence to the importance of TRIM28 in tumor progression. High levels of TRIM28 correlated with a significantly lower survival rate in patients with ovarian, gastric and pancreatic cancer [10,16,27,28]. There was a positive correlation between TRIM28 expression and glioma malignancy [29,30].…”

Section: Discussionmentioning

confidence: 86%

“…Meanwhile, TRIM28 could serve as a SUMO/ubiquitin E3 ligas and regulate apoptosis [14]. To date, many studies have indicated that TRIM28 plays an important role in the proliferation and migration of tumor cells, and higher levels of TRIM28 expression have been observed in liver, gastric, lung, breast, pancreatic, ovarian and prostate cancer [1,5,6,8,10,11,13,14,17,18,[20][21][22]. Despite many efforts to elucidate the cellular functions and associated molecular mechanisms of TRIM28, the relation between TRIM28 and OS has not been reported.…”

Section: Introductionmentioning

confidence: 99%

TRIM28 is Overexpressed in Osteosarcoma and Associated with Tumor Progression

Cui¹,

Wang²,

Yang³

et al. 2017

Preprint

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Tripartite motif containing 28 (TRIM28) is a transcriptional co-factor with pleiotropic biological activities, especially in tumor cells. In this study, expression levels of TRIM28 in osteosarcoma (OS) tissues and the correlations with clinicopathological variables were investigated in 87 OS cases, meanwhile, cell and animal experiments were performed to detect the biological functions of TRIM28. The results showed that TRIM28 was overexpressed in OS tissues compared with normal bones, and TRIM28 expression correlated significantly with tumor diameter (χ2 = 4.06, p=0.04), metastasis (χ2 =11.10, p< 0.01) and clinical stage (χ2 =15.50, p< 0.01). Furthermore, patients with high TRIM28 level always had poor survival (p < 0.01). Functionally, TRIM28 knockdown significantly inhabited cell ability of proliferation and migration in OS cell lines of in vitro and in vivo experiments. Additionally, TRIM28 could significantly inhibited E-cadherin expression in reducing the stability of the TRIM28 mRNA. Therefore, TRIM28 overexpression was correlated with malignant progression of OS and poor survival of OS patients, and TRIM28 pathway may be a therapeutic target for OS.

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High Levels of KAP1 Expression Are Associated with Aggressive Clinical Features in Ovarian Cancer

Cited by 46 publications

References 26 publications

NADPH accumulation is responsible for apoptosis in breast cancer cells induced by fatty acid synthase inhibition

NADPH accumulation is responsible for apoptosis in breast cancer cells induced by fatty acid synthase inhibition

<p>GLUT5 increases fructose utilization in ovarian cancer</p>

TRIM28 is Overexpressed in Osteosarcoma and Associated with Tumor Progression

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