SPARCL1 suppresses metastasis in prostate cancer

Xiang, Yuzhu; Qiu, Qingchao; Jiang, Ming; Jin, Renjie; Lehmann, Brian D.; Strand, Douglas W.; Jovanović, Bojana; DeGraff, David J.; Zheng, Yi; Yousif, Dina A.; Simmons, Christine Q.; Case, Thomas C.; Jia, Yi; Cates, Justin M.; Virostko, John; He, Xiu‐Sheng; Jin, Xunbo; Hayward, Simon W.; Matusik, Robert J.; George, Alfred L.; Yi, Yajun

doi:10.1016/j.molonc.2013.07.008

Cited by 33 publications

(33 citation statements)

References 43 publications

(64 reference statements)

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“…According to the results of our meta-analysis, the overexpression of SPARCL1 may reduce cancer metastasis (including lymph node and distant metastases) which contributes to survival benefits. Furthermore, some scientists have concluded that SPARCL1 gene plays a suppressor role in tumor metastasis in various cancers [24, 33, 34]. Our results also showed that the expression of SPARCL1 indicated better tumor differentiation (OR=2.21, P =0.000).…”

Section: Discussionsupporting

confidence: 73%

SPARCL1, a Novel Prognostic Predictive Factor for GI Malignancies: a Meta-Analysis

Cui

Zheng

et al. 2017

Cell Physiol Biochem

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Background/Aims: Secreted protein acidic and rich in cysteines-like 1 (SPARCL1) is abnormally expressed in gastrointestinal (GI) malignancies. However, the correlation between SPARCL1 expression and the prognosis of patients remains unknown. Therefore, we performed a meta-analysis to investigate the potential value of SPARCL1 as a prognostic predictive marker for GI malignancies. Methods: The PubMed, Embase, EBSCO, CNKI, and Wanfang databases were systematically searched for studies examining SPARCL1 and clinicopathological features, including the prognoses of patients. Hazard ratios (HRs) and odds ratios (ORs) from individual studies were calculated and pooled using a random-effects or fix-effects model. Heterogeneity and publication bias analyses were performed. Results: Data from 8 studies, including a total of 2,356 patients, were summarized. The expression of SPARCL1 suggested a better prognosis (HR=0.57, 95% CI: 0.445-0.698, P=0.000) and was associated with clinicopathological features of GI malignancies, including distant metastasis (OR=0.44, 95% CI: 0.23-0.85, P=0.014), lymph node metastasis (OR=0.56, 95% CI: 0.39–0.81, P=0.002) and tumor differentiation (OR=2.21, 95% CI: 1.82–2.69, P=0.000). Subgroup analyses based on cancer type revealed that the expression of SPARCL1 had no effect on lymph node metastasis in colorectal cancer, and it did not influence tumor differentiation in gastric cancer. Egger’s test showed no evidence of publication bias (all P>0.05). Conclusion: SPARCL1 could be a novel prognostic predictive factor for GI malignancies. The expression of SPARCL1 could influence the clinicopathological features of GI malignancies. Further large-scale studies are essential to confirm SPARCL1’s prognostic predictive value, and more fundamental experimental studies are needed to illustrate the mechanisms.

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Section: Discussionsupporting

confidence: 73%

SPARCL1, a Novel Prognostic Predictive Factor for GI Malignancies: a Meta-Analysis

Cui

Zheng

et al. 2017

Cell Physiol Biochem

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“…While several functional studies support that SPARCL1 restricts tumor growth and progression (4, 6, 7), the role for SPARCL1 in prostate cancer remains poorly understood. The correlation between SPARCL1 loss and aggressiveness of clinically localized prostate cancer suggests that SPARCL1 may function as a barrier to tumor initiation and progression in the prostate (4).…”

Section: Introductionmentioning

confidence: 99%

“…Consistent with this, overexpression of SPARCL1 in colon cancer cells suppressed growth of subcutaneous xenografts (6). While SPARCL1 has been shown to inhibit in vitro proliferation of colon cancer (6) and HeLa (8) cells, other studies support that SPARCL1 may not regulate cellular proliferation in the prostate (4, 7). Alternatively, SPARCL1 has been shown in multiple models to inhibit processes integral to both local and metastatic progression such as cancer cell adhesion, migration and invasion (4, 6, 7, 9, 10).…”

Section: Introductionmentioning

confidence: 99%

“…While SPARCL1 has been shown to inhibit in vitro proliferation of colon cancer (6) and HeLa (8) cells, other studies support that SPARCL1 may not regulate cellular proliferation in the prostate (4, 7). Alternatively, SPARCL1 has been shown in multiple models to inhibit processes integral to both local and metastatic progression such as cancer cell adhesion, migration and invasion (4, 6, 7, 9, 10). Two recent reports demonstrate that SPARCL1 suppresses tumor nodule formation in visceral organs following intravenous injection (6, 7).…”

Section: Introductionmentioning

confidence: 99%

“…Alternatively, SPARCL1 has been shown in multiple models to inhibit processes integral to both local and metastatic progression such as cancer cell adhesion, migration and invasion (4, 6, 7, 9, 10). Two recent reports demonstrate that SPARCL1 suppresses tumor nodule formation in visceral organs following intravenous injection (6, 7). While these studies collectively support that SPARCL1 constrains cancer growth; the precise role of SPARCL1 in the step-wise progression from prostate tumor initiation through localized progression has not been definitively examined in an autochthonous model.…”

Section: Introductionmentioning

confidence: 99%

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Androgen-Regulated SPARCL1 in the Tumor Microenvironment Inhibits Metastatic Progression

et al. 2015

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Prostate cancer is a leading cause of cancer death in men due to the subset of cancers that progress to metastasis. Prostate cancers are thought to be hardwired to androgen receptor (AR) signaling, but AR-regulated changes in the prostate that facilitate metastasis remain poorly understood. We previously noted a marked reduction in Secreted protein, acidic and rich in cysteine-like 1 (SPARCL1) expression during invasive phases of androgen-induced prostate growth, suggesting that this may be a novel invasive program governed by AR. Herein, we show that SPARCL1 loss occurs concurrently with AR amplification or overexpression in patient based data. Mechanistically, we demonstrate that SPARCL1 expression is directly suppressed by androgen-induced AR activation and binding at the SPARCL1 locus via an epigenetic mechanism, and these events can be pharmacologically attenuated with either AR antagonists or HDAC inhibitors. We establish using the Hi-Myc model of prostate cancer that in Hi-Myc/Sparcl1−/− mice, SPARCL1 functions to suppress cancer formation. Moreover, metastatic progression of Myc-CaP orthotopic allografts is restricted by SPARCL1 in the tumor microenvironment. Specifically, we show that SPARCL1 both tethers to collagen in the extracellular matrix (ECM) and binds to the cell's cytoskeleton. SPARCL1 directly inhibits the assembly of focal adhesions thereby constraining the transmission of cell traction forces. Our findings establish a new insight into AR-regulated prostate epithelial movement and provide a novel framework whereby, SPARCL1 in the ECM microenvironment restricts tumor progression by regulating the initiation of the network of physical forces that may be required for metastatic-invasion of prostate cancer.

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Titanium(IV) immobilized affinity chromatography facilitated phosphoproteomics analysis of salivary extracellular vesicles for lung cancer

et al. 2022

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SPARCL1 suppresses metastasis in prostate cancer

Cited by 33 publications

References 43 publications

SPARCL1, a Novel Prognostic Predictive Factor for GI Malignancies: a Meta-Analysis

SPARCL1, a Novel Prognostic Predictive Factor for GI Malignancies: a Meta-Analysis

Androgen-Regulated SPARCL1 in the Tumor Microenvironment Inhibits Metastatic Progression

Titanium(IV) immobilized affinity chromatography facilitated phosphoproteomics analysis of salivary extracellular vesicles for lung cancer

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