Proinflammatory Cytokines in Prostate Cancer Development and Progression Promoted by High-Fat Diet

Xu, Hua; Hu, Mengbo; Bai, Peide; Zhu, Wenhui; Liu, Sheng-hua; Hou, Jiayun; Xiong, Zhenggang; Ding, Qiang; Jiang, Haowen

doi:10.1155/2015/249741

Cited by 34 publications

(35 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Under these conditions, tumors engrafted in HFD-fed animals exhibited an accelerated growth rate compared with LFD-fed mice, suggesting an association between high calorie intake from fat and prostate cancer growth. Of note, these results are consistent with previous studies in TRAMP mice showing that HFD can promote prostate tumor formation, likely due to an increase in cytokines (27), and tumor growth compared with lean mice (28). Similarly, these data are also in agreement with previous reports showing that an HFD could increase the tumor growth in LNCaP xenografts, wherein this effect was due to high levels of diet-induced insulin/IGF1 (29,30).…”

Section: Discussionsupporting

confidence: 92%

Metformin Reduces Prostate Tumor Growth, in a Diet-Dependent Manner, by Modulating Multiple Signaling Pathways

Sarmento‐Cabral

L‐López

Gahete

et al. 2017

Molecular Cancer Research

View full text Add to dashboard Cite

Prostate-cancer is strongly influenced by obesity, wherein metformin could represent a promising treatment; however, the endocrine metabolic/cellular/molecular mechanisms underlying these associations and effects are still unclear. To determine the beneficial antitumoral effects of metformin on prostate cancer progression/aggressiveness and the relative contribution of high-fat diet (HFD; independently of obesity), we used HFD-fed immunosuppressed mice inoculated with PC3 cells (which exhibited partial resistance to diet-induced obesity) compared with low-fat diet (LFD)-fed control mice. Moreover, gene expression analysis was performed on cancer-associated genes in the xenografted tumors, and the antitumorigenic role of metformin on tumoral (PC3/22Rv1/LNCaP) and normal (RWPE1) prostate cells was evaluated. The results demonstrate that HFD is associated with enhanced prostate cancer growth irrespective of body weight gain and endocrine metabolic dysregulations and that metformin can reduce prostate cancer growth under LFD but more prominently under HFD, acting through the modulation of several tumoral-associated processes (e.g., cell cycle, apoptosis, and/or necrosis). Moreover, the actions observed could be mediated by the modulation of the local expression of GH/IGF1 axis components. Finally, it was demonstrated that metformin had disparate effects on proliferation, migration, and prostate-specific antigen secretion from different cell lines. Altogether, these data reveal that metformin inhibits prostate cancer growth under LFD and, specially, under HFD conditions through multiple metabolic/tumoral signaling pathways. The current study linking dietary influence on metformin-regulated signaling pathways and antitumoral response provides new and critical insight on environment-host interactions in cancer and therapy. .

show abstract

Section: Discussionsupporting

confidence: 92%

Metformin Reduces Prostate Tumor Growth, in a Diet-Dependent Manner, by Modulating Multiple Signaling Pathways

Sarmento‐Cabral

L‐López

Gahete

et al. 2017

Molecular Cancer Research

View full text Add to dashboard Cite

show abstract

“…These inflammatory markers are also associated with PCa promotion and progression both in clinical and in vitro studies . Notably, IL‐6 secreted by PPAT from patients with PCa was present at >375 times greater concentration than in the matched patient serum, and significantly with the disease pathological grade .…”

Section: Potential Mechanistic Links Between Peri‐prostatic Adipose Tmentioning

confidence: 96%

Peri‐prostatic adipose tissue: the metabolic microenvironment of prostate cancer

et al. 2018

View full text Add to dashboard Cite

Emerging data have linked certain features of clinical prostate cancer (PCa) to obesity and, more specifically, increased adiposity. Whereas the large number of clinical studies and meta-analyses that have explored the associations between PCa and obesity have shown considerable variability, particularly in relation to prostate cancer risk, there is an accumulating weight of evidence consistently linking obesity to greater aggressiveness of disease. In probing this association mechanistically, it has been posited that peri-prostatic adipose tissue (PPAT), a significant component of the prostate microenvironment, may be a critical source of fatty acids and other mitogens and thereby influences PCa pathogenesis and progression. Notably, several recent studies have identified secreted factors from both PPAT and PCa that potentially mediate the two-way communication between these intimately linked tissues. In the present review, we summarize the available literature regarding the relationship between PPAT and PCa, including the potential biological mediators of that relationship, and explore emerging areas of interest for future research endeavours.

show abstract

“…14,15 And the levels of IL-18 and IL-1β is associated with cellular inflammation thought to be linked to prostate carcinogenesis and prostate cancer development. [15][16][17][18][19][20][21] In consequence, matrine combined with docetaxel also maybe inhibit tumor cells by promoting the levels of IL-18 and IL-1β and suppressing inflammation.…”

Section: Discussionmentioning

confidence: 99%

<p>The Effects of Matrine in Combination with Docetaxel on Castration-Resistant (Androgen-Independent) Prostate Cancer</p>

Li¹,

Xu²,

He³

et al. 2019

CMAR

View full text Add to dashboard Cite

Background: Matrine (MAT) exhibits higher efficacy of chemotherapy when it is combined with other chemotherapeutic drugs; however, the therapeutic efficacy of matrine in combination with docetaxel (DOC) for prostate cancer, or even androgen-independent prostate cancer, remains poorly understood and the underlying molecular mechanisms have not yet been clearly defined. In the present study, we investigated whether matrine combined with docetaxel can strengthen anti-cancer effect. Methods: In this study, 7 groups were established, including (1) blank control group (cells).(2) 0.1 g/L MAT group, (3) 0.5 g/L MAT group, (4) 0.1 g/L MAT+ 50 μg/L DOC group, (5) 0.5 g/L MAT+ 50 μg/L DOC group, (6) 0.1 g/L MAT+ 100 μg/L DOC group, and (7) 0.5 g/L MAT+ 100 μg/L DOC group. MTS assay was performed to detect the anti-proliferative effects of each group on DU145 and PC-3 cells. At the same time, Transwell assay was performed to detect anti-migrative and anti-invasive effects of each group on DU145 and PC-3 cells. Biochemical colorimetric method and enzyme-linked immunosorbent assay were performed to detect the levels of LDH, IL-1β and IL-18 of each group on DU145 and PC-3 cells. Flow cytometry (FCM) assay was used to do the apoptosis analysis on DU145 and PC-3 cells of each group. At last, Western blot analysis was performed to investigate the expression levels of caspase1 in cells of each group. Statistical analyses were performed with SPSS 17.0 (SPSS Inc, USA) software, and one-way ANOVA and Fisher's exact test was taken. Results: MTS assay showed that matrine combined with docetaxel could inhibit both DU145 and PC-3 cells' proliferation in a dose-and time-dependent manner. Transwell assay showed that matrine combined with docetaxel could inhibit both DU145 and PC-3 cells' migration and invasion in a dose-and time-dependent manner. The levels of LDH, IL-1β and IL-18 of matrine combined with docetaxel-treated DU145 and PC-3 cells were significantly increased, compared with the untreated control cells. Flow cytometry, as well as Annexin-V/PI staining, showed a significant and dose-dependent increase in the number of early, as well as late-stage apoptotic cells in both DU145 and PC-3 cells compared with the untreated control cells. Western blot analysis showed that matrine combined with docetaxel treatment led to the expression of caspase1 in both DU145 and PC-3 cells. Conclusion: It may be more effective to use matrine in combination with docetaxel to treat androgen-resistant prostate cancer because matrine can help to affect proliferation, migration, invasion, apoptosis, metabolism, and have anti-inflammation effect on the tumor cells.

show abstract

Proinflammatory Cytokines in Prostate Cancer Development and Progression Promoted by High-Fat Diet

Cited by 34 publications

References 45 publications

Metformin Reduces Prostate Tumor Growth, in a Diet-Dependent Manner, by Modulating Multiple Signaling Pathways

Metformin Reduces Prostate Tumor Growth, in a Diet-Dependent Manner, by Modulating Multiple Signaling Pathways

Peri‐prostatic adipose tissue: the metabolic microenvironment of prostate cancer

<p>The Effects of Matrine in Combination with Docetaxel on Castration-Resistant (Androgen-Independent) Prostate Cancer</p>

Contact Info

Product

Resources

About