Expression of SDF-1 and CXCR4 transcript variants and CXCR7 in epithelial ovarian cancer

Jaszczyńska-Nowinka, Karolina; Ruciński, Marcin; Ziółkowska, Agnieszka; Markowska, Anna; Malendowicz, Ludwik K.

doi:10.3892/ol.2014.1897

Cited by 8 publications

(7 citation statements)

References 36 publications

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“…No changes in CXCR4 and CXCR7 expression level are observed. Elevated plasma SDF-1α level in epithelial ovarian cancer patients is not associated with the presence of tumors and/or metastases, however reflects a general response to the disease [72].…”

Section: Introductionmentioning

confidence: 99%

Microvesicles and chemokines in tumor microenvironment: mediators of intercellular communications in tumor progression

et al. 2019

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Increasing evidence indicates that the ability of cancer cells to convey biological information to recipient cells within the tumor microenvironment (TME) is crucial for tumor progression. Microvesicles (MVs) are heterogenous vesicles formed by budding of the cellular membrane, which are secreted in larger amounts by cancer cells than normal cells. Recently, several reports have also disclosed that MVs function as important mediators of intercellular communication between cancerous and stromal cells within the TME, orchestrating complex pathophysiological processes. Chemokines are a family of small inflammatory cytokines that are able to induce chemotaxis in responsive cells. MVs which selective incorporate chemokines as their molecular cargos may play important regulatory roles in oncogenic processes including tumor proliferation, apoptosis, angiogenesis, metastasis, chemoresistance and immunomodulation, et al. Therefore, it is important to explore the association of MVs and chemokines in TME, identify the potential prognostic marker of tumor, and develop more effective treatment strategies. Here we review the relevant literature regarding the role of MVs and chemokines in TME.

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Section: Introductionmentioning

confidence: 99%

Microvesicles and chemokines in tumor microenvironment: mediators of intercellular communications in tumor progression

et al. 2019

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“…Additionally, the expression of CXCL12, CXCR4, and CXCR7 in Figure 6 The role of CXCL12 and its receptors CXCR4, CXCR7 on Apoptosis of KGN cells. Apoptosis rate of KGN cells after 100 ng/mL rhCXCL12 (CXCL12, n = 6), 100 ng/mL rhCXCL12 with 1 μg/mL CXCR4 antagonist AMD3100 (CXCL12 + AMD3100, n = 6), 100 ng/mL rhCXCL12 with 10 μg/mL anti-CXCR7 neutralizing antibody (CXCL12 + Anti-CXCR7, n = 6), 100 ng/mL rhCXCL12 with 10 μg/mL isotype IgG (CXCL12 + IgG, n = 6) incubation for 24 h. *P < 0.05. human epithelial ovarian cancer has been examined (Jaszczynska-Nowinka et al 2014). Meanwhile, the joint expression of CXCL12 and its receptors CXCR4 and CXCR7 in the ovary of PCOS rat is shown for the first time in the present study.…”

Section: Discussionmentioning

confidence: 61%

CXCL12 and its receptors regulate granulosa cell apoptosis in PCOS rats and human KGN tumor cells

Jin

Ren

et al. 2021

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Polycystic ovary syndrome (PCOS) is a common endocrine disorder accompanied by chronic low-grade inflammation; its etiology is still undefined. This study investigated the expression of CXCL12, CXCR4, and CXCR7 in PCOS rats and their role in regulation of apoptosis. To accomplish this, we established an in vivo PCOS rat model and studied KGN cells (human ovarian granulosa cell line) in vitro. In PCOS rats, the ovarian expression of CXCL12, CXCR4, and CXCR7 was reduced, and the apoptosis rate of granulosa cells was increased, accompanied by decreased expression of BCL2 and increased expression of BAX and cleaved CASPASE3 (CASP3). We further showed that recombinant human CXCL12 treatment upregulated BCL2, downregulated BAX, and cleaved CASP3 in KGN cells to inhibit their apoptosis in a concentration-dependent manner; moreover, the effect of CXCL12 was weakened by CXCR4 antagonist AMD3100 and anti-CXCR7 neutralizing antibody. In conclusion, PCOS rats showed decreased CXCL12, CXCR4, and CXCR7 expression and increased apoptosis rate of ovarian granulosa cells. Further, in human KGN cells, CXCL12 regulated the expression of BAX, BCL2, and cleaved CASP3 to inhibit apoptosis through CXCR4- and CXCR7-mediated signal transmission. These findings may provide a theoretical and practical basis for illuminating the role of proinflammatory cytokines in the pathogenesis of PCOS.

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“…The SDF-1 concentration gradient is a driving force for stem cell migration [41]. Studies showed that the expression of SDF-1 was present at extremely low levels or even not originally identi ed in normal ovaries [43,44]. However, after injury, the chemokine SDF-1 level increased in tissue, which is critical for the chemotaxis of stem cells homing to the injured or ischemic tissue [24,27,[45][46][47][48][49].…”

Section: Discussionmentioning

confidence: 99%

Important Role of SDF-1/CXCR4 Axis in the Homing of Systemically Transplanted Human Amnion-Derived Mesenchymal Stem Cells (Had-Mscs) to Ovaries in Rats with Chemotherapy-Induced Premature Ovarian Insufficiency (POI)

Hou

Liu³

et al. 2021

Preprint

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Background: Chemotherapy can induce premature ovarian insufficiency (POI). POI causes multiple sequelae and is currently incurable. Our previous studies have demonstrated that systemically transplanted human amnion-derived mesenchymal stem cells (hAD-MSCs) can home to chemotherapy-induced POI ovaries, and thus reduce ovarian injury and improve ovarian function in rats with POI. However, the cellular mechanisms that direct the migration and homing of hAD-MSCs to chemotherapy-induced POI ovaries are barely understood. This study was to investigate the role of SDF-1/CXCR4 axis in the migration and homing of systemically transplanted hAD-MSCs to chemotherapy-induced POI ovaries and its relevant downstream signaling pathways.Methods: CXCR4 expression in hAD-MSCs was tested by western blot and immunofluorescence assay. hAD-MSC migration was tested by transwell migration assay. SDF-1 level in rats was detected by ELISA. 72 of female SD rats were randomly divided into the control, POI, hAD-MSCs and hAD-MSCs+AMD3100 groups. POI rat models were established by intraperitoneal injection of cyclophosphamide. For the inhibitor treatment, hAD-MSCs were pretreated with AMD3100 before transplantation. hAD-MSCs labeled with PKH26 were injected into the tail vein of POI rats at 24 h after chemotherapy. After hAD-MSC transplantation, the homing of hAD-MSCs in ovaries, and ovarian function and pathological changes were examined. To further investigate molecular mechanisms, PI3K/Akt and ERK1/2 signaling pathways were detected. Results: hAD-MSCs expressed CXCR4. SDF-1 induced hAD-MSC migration in vitro. SDF-1 levels in ovaries and serum significantly increased in POI rats induced by chemotherapy, and POI ovaries attracted the homing of hAD-MSCs expressing CXCR4. The block of SDF-1/CXCR4 axis with AMD3100 can significantly reduce the number of hAD-MSCs homing to the POI ovaries, and further reduce their efficacy in POI treatment. The binding of SDF-1 to CXCR4 activated PI3K/Akt signaling pathway, and LY294002 significantly inhibited hAD-MSC migration induced by SDF-1 in vitro. Moreover, inhibition of PI3K/Akt signaling pathway significantly reduced the number of systemically transplanted hAD-MSCs homing to chemotherapy-induced POI ovaries in rats.Conclusions: SDF-1/CXCR4 axis partially mediates the migration and homing of systemically transplanted hAD-MSCs to chemotherapy-induced POI ovaries in rats, and PI3K/Akt signaling pathway might be involved in the migration and homing of hAD-MSCs mediated by SDF-1/CXCR4 axis.

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Expression of SDF-1 and CXCR4 transcript variants and CXCR7 in epithelial ovarian cancer

Cited by 8 publications

References 36 publications

Microvesicles and chemokines in tumor microenvironment: mediators of intercellular communications in tumor progression

Microvesicles and chemokines in tumor microenvironment: mediators of intercellular communications in tumor progression

CXCL12 and its receptors regulate granulosa cell apoptosis in PCOS rats and human KGN tumor cells

Important Role of SDF-1/CXCR4 Axis in the Homing of Systemically Transplanted Human Amnion-Derived Mesenchymal Stem Cells (Had-Mscs) to Ovaries in Rats with Chemotherapy-Induced Premature Ovarian Insufficiency (POI)

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