Expression and histopathological correlation of CCR9 and CCL25 in ovarian cancer

Singh, Rajesh; Stockard, Cecil R.; Grizzle, William E.; Lillard, James W.; Singh, Shailesh

doi:10.3892/ijo.2011.1059

Cited by 32 publications

(35 citation statements)

References 30 publications

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“…[10][11][12][13][14][15][16][17] We found that CXCR3 expression in LNCaP cells was decreased after 6 hr of AG treatment, but this suppressive effect was short lived and the receptor expression recovered after 24 hr. In case of PC3 and DU-145 cells, reduced expression of CXCR3 was maintained from 6 to 24 hr after AG treatment.…”

Section: Ag Modulates Chemokine Expression In Pca Cellsmentioning

confidence: 78%

“…Cytokines mediated signals can cross talk with chemokines and multiple chemokine-receptors are shown to be associated with tumor progression and metastasis. [7][8][9][10][11][12][13][14][15][16][17] Additionally, cell cycle regulation is governed by calcium flux, which in turn is altered by chemokine signaling. In this manuscript we have presented evidence that AG exerts its anticancer effects by modulating cell cycle as well as chemokine receptors (CXCR3 and CXCR7) and their common ligand CXCL11 in PCa cells.…”

Section: Introductionmentioning

confidence: 99%

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Andrographolide inhibits prostate cancer by targeting cell cycle regulators, CXCR3 and CXCR7 chemokine receptors

et al. 2016

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Despite state of the art cancer diagnostics and therapies offered in clinic, prostate cancer (PCa) remains the second leading cause of cancer-related deaths. Hence, more robust therapeutic/preventive regimes are required to combat this lethal disease. In the current study, we have tested the efficacy of Andrographolide (AG), a bioactive diterpenoid isolated from Andrographis paniculata, against PCa. This natural agent selectively affects PCa cell viability in a dose and time-dependent manner, without affecting primary prostate epithelial cells. Furthermore, AG showed differential effect on cell cycle phases in LNCaP, C4-2b and PC3 cells compared to retinoblastoma protein (RB ¡/¡ ) and CDKN2A lacking DU-145 cells. G2/M transition was blocked in LNCaP, C4-2b and PC3 after AG treatment whereas DU-145 cells failed to transit G1/S phase. This difference was primarily due to differential activation of cell cycle regulators in these cell lines. Levels of cyclin A2 after AG treatment increased in all PCa cells line. Cyclin B1 levels increased in LNCaP and PC3, decreased in C4-2b and showed no difference in DU-145 cells after AG treatment. AG decreased cyclin E2 levels only in PC3 and DU-145 cells. It also altered Rb, H3, Wee1 and CDC2 phosphorylation in PCa cells. Intriguingly, AG reduced cell viability and the ability of PCa cells to migrate via modulating CXCL11 and CXCR3 and CXCR7 expression. The significant impact of AG on cellular and molecular processes involved in PCa progression suggests its potential use as a therapeutic and/or preventive agent for PCa.

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Section: Ag Modulates Chemokine Expression In Pca Cellsmentioning

confidence: 78%

Section: Introductionmentioning

confidence: 99%

Andrographolide inhibits prostate cancer by targeting cell cycle regulators, CXCR3 and CXCR7 chemokine receptors

et al. 2016

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“…CCR9 with its natural ligand CCL25 has been shown to be highly expressed by prostate cancer cells (4). It has been shown to affect cancer cell migration, invasion, and MMP expression which together are involved in cancer cell metastasis (5,7). Further, it is known to upregulate antiapoptotic proteins such as P13K, AKT, ERK1/2 and GSK-3…”

Section: Resultsmentioning

confidence: 99%

“…1. Isolate, expand, and prepare a stock of frozen ASCs from Glipr1 WT and KO male mice (6)(7)(8)(9)(10)(11)(12) months). 2.…”

Section: Aim 2: Study the Interactions Between Ascs Isolated Frommentioning

confidence: 99%

Androgenic Regulation of White Adipose Tissue-Prostate Cancer Interactions

Thompson¹

2012

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATE May 2012 REPORT TYPE PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBERUniversity of Texas MD Anderson Cancer Center Houston, TX 77030 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTES ABSTRACTAdipocyte stromal cells from WAT of both Glipr1 wild type adult males and Glipr1 knock out adult males were isolated and used for coculturing experiment. Coculturing prostate cancer cells (VCaP, RM-9, PC-3) with ASCs from WAT of Glipr1 KO and Glipr1 WT resulted in increased growth of the cancer cells compared to the cells grown without the ASCs. Moreover, the prostate cancer cells grown with Glipr1 KO ASCs resulted in higher cell growth rate compared to the cells grown with Glipr1 WT ASCs. Similar results were found after the prostate cancer cells were incubated with ASCs-CM from both Glipr1 KO and WT. The cells incubated with Glipr1 KO ASCs-CM resulted in higher cell growth number compared to the cells grown with Glipr1 WT ASCs-CM, indicating the presence of differential levels of factors that promote cell growth. When the ASCs-CM from Glipr1 WT and KO were analyzed and compared, we detected numerous factors that promote tumor cell growth and invasion. As expected, the levels of these factors that promote cancer cell growth and invasion were much higher in Glipr1 KO ASCs-CM than in Glipr1 WT ASCs-CM. -/-knockout (KO) mice. We are testing our hypothesis that the biologic activity of WAT is affected by castration and that although the acute effects of castration (e.g., GLIPR1 induction) may suppress cancer-promoting adipokines, long-term ADT results in monocyte infiltration and the generation of WAT-associated macrophages (WAMs). WAMs, in turn, produce cytokines and promote the growth and survival of growth factor-expressing ASCs, which enter the systemic circulation and promote PCa progression. An important note is ...

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“…The natural ligand of CCR9, CCL25, is a thymusexpressed chemokine, which has been found primarily in the involvement of immune homeostasis and then in human solid tumors such as colorectal, prostate, ovarian, and breast cancers with relation to tumor invasion and metastasis (Singh et al, 2004;Svensson and Agace, 2006;Johnson-Holiday et al, 2011;Singh et al, 2011;Chen et al, 2012). However, the study of the CCL25/CCR9 axis on lung cancer is limited; so far, only one study has found that its expression correlated with aggressiveness and mediated key steps of metastasis in clinical samples and cell lines of NSCLC, especially in adenocarcinomas compared with squamous cell carcinomas, due to differential expression of matrix metalloproteinases and tissue inhibitor of metalloproteinases under the influence of CCL25 (Gupta et al, 2014).…”

Section: Ccl25/ccr9mentioning

confidence: 99%

Chemokines and their receptors in lung cancer progression and metastasis

Cheng

Shi

Yuan

et al. 2016

J. Zhejiang Univ. Sci. B

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Lung cancer is the leading cause of cancer-related mortality around the world. Despite advancements in diagnosis, surgical techniques, and neoadjuvant chemoradiotherapy over the last decade, the mortality rate is still high and the 5-year survival is a dismal 15%. Fortunately, early detection by low-dose computed tomography (LDCT) scans has reduced mortality by 20%; yet, overall, 5-year-survival remains low at less than 20%. Therefore, in order to ameliorate this situation, a thorough understanding of the underlying molecular mechanisms is urgently needed. Chemokines and their receptors, crucial microenvironmental factors, play important roles in lung tumor genesis, progression, and metastasis, and exploring the mechanisms of this might bring new insights into early diagnosis and precisely targeted treatment. Consequently, this review will mainly focus on recent advancements on the axes of chemokines and their receptors of lung cancer.

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Expression and histopathological correlation of CCR9 and CCL25 in ovarian cancer

Cited by 32 publications

References 30 publications

Andrographolide inhibits prostate cancer by targeting cell cycle regulators, CXCR3 and CXCR7 chemokine receptors

Andrographolide inhibits prostate cancer by targeting cell cycle regulators, CXCR3 and CXCR7 chemokine receptors

Androgenic Regulation of White Adipose Tissue-Prostate Cancer Interactions

Chemokines and their receptors in lung cancer progression and metastasis

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