The Role of p-STAT3 as a Prognostic and Clinicopathological Marker in Colorectal Cancer: A Systematic Review and Meta-Analysis

Ji, Kun; Zhang, Mingxuan; Chu, Q.; Gan, Yong; Ren, Hui; Zhang, Liyan; Wang, Liwei; Li, Xiaoxiu; Wang, Wei

doi:10.1371/journal.pone.0160125

Cited by 43 publications

(35 citation statements)

References 43 publications

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“…In this model, MSCs promoted intestinal regeneration after irradiation in agreement with the multiple therapeutic effects of MSCs including stimulation of proliferation, inhibition of apoptosis, stimulation of angiogenesis and a large range of anti‐inflammatory activities . Our results highlights a dynamic progression of ECM remodeling with a balance toward fibrogenesis in irradiated tissues which is counteracted by MSC administration coherent with previous findings . The regenerative capacity of MSCs was mediated by secretion of HGF and VEGF.…”

Section: Discussionsupporting

confidence: 90%

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Mesenchymal Stem Cell Administration Attenuates Colon Cancer Progression by Modulating the Immune Component within the Colorectal Tumor Microenvironment

François

Usunier

Forgue‐Lafitte

et al. 2018

Stem Cells Translational Medicine

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We here determine the influence of mesenchymal stem cell (MSC) therapy on the progression of solid tumors. The influence of MSCs was investigated in human colorectal cancer cells as well as in an immunocompetent rat model of colorectal carcinogenesis representative of the human pathology. Treatment with bone marrow (BM)‐derived MSCs significantly reduced both cancer initiation and cancer progression by increasing the number of tumor‐free animals as well as decreasing the number and the size of the tumors by half, thereby extending their lifespan. The attenuation of cancer progression was mediated by the capacity of the MSCs to modulate the immune component. Specifically, in the adenocarcinomas (ADKs) of MSC‐treated rats, the infiltration of CD68+ monocytes/macrophages was 50% less while the presence of CD3+ lymphocytes increased almost twofold. The MSCs reprogrammed the macrophages to become regulatory cells involved in phagocytosis thereby inhibiting the production of proinflammatory cytokines. Furthermore, the MSCs decreased NK (Natural Killer) and rTh17 cell activities, Treg recruitment, the presence of CD8+ lymphocytes and endothelial cells while restoring Th17 cell activity. The expression of miR‐150 and miR‐7 increased up to fivefold indicating a likely role for these miRNAs in the modulation of tumor growth. Importantly, MSC administration limited the damage of healthy tissues and attenuated tumor growth following radiotherapy. Taken together, we here show that that MSCs have durable action on colon cancer development by modulating the immune component of the tumor microenvironment. In addition, we identify two miRNAs associated with the capacity of MSCs to attenuate cancer growth. Stem Cells Translational Medicine 2019;8:285&300

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Section: Discussionsupporting

confidence: 90%

“…The first injection was carried out 2 weeks after the last MNNG injection to prevent early damages. The doses of MSCs as well as the repeated injections were chosen according to our previous study which demonstrated a cumulative effect of repeated MSC injections . The presence of exogenous MSCs in the colon was verified using an eGFP tag (Fig.…”

Section: Resultsmentioning

confidence: 99%

Mesenchymal Stem Cell Administration Attenuates Colon Cancer Progression by Modulating the Immune Component within the Colorectal Tumor Microenvironment

François

Usunier

Forgue‐Lafitte

et al. 2018

Stem Cells Translational Medicine

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“…[25][26][27] As reported, JAK-STAT signaling is associated with tumors via upregulating Bcl-2, cyclin D1, and c-Myc. 30,31 JAK-STAT3 is involved in multiple biological processes; hence, it is associated with tumor progression. 30,31 JAK-STAT3 is involved in multiple biological processes; hence, it is associated with tumor progression.…”

Section: Discussionmentioning

confidence: 99%

LINC00346 promotes hepatocellular carcinoma progression via activating the JAK‐STAT3 signaling pathway

Yin

Zheng

Zhang

et al. 2019

J of Cellular Biochemistry

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Hepatocellular carcinoma (HCC) remains the most common malignant tumor worldwide. Long noncoding RNAs can modulate various tumorigenic processes. In addition, growing evidence has indicated tha the Janus kinase–signal transducer and activator of transcription (JAK‐STAT) pathway is activated in multiple cancers, including HCC. Recently, it was found that LINC00346 can participate in several cancers. Nevertheless, the biological roles of LINC00346 in HCC have been barely investigated. In this study, the function of LINC00346 was specifically concentrated upon. We observed that LINC00346 was obviously elevated in HCC cells (Bel7404, Huh‐6, HepG2, and QGY‐7703 cells). Then, Bel7404 and HepG2 cells were overexpressed with LINC00346. Overexpression of LINC00346 repressed HCC cell survival and cell proliferation. In addition, apoptosis of Bel7404 and HepG2 cells was triggered by LINC00346 upregulation. Bel7404 and HepG2 cell cycle was arrested in the G1 phase by LINC00346. Meanwhile, we conducted wound‐healing assay and Transwell invasion assays. As shown, we observed that the migratory and invasive capacities of Bel7404 and HepG2 cells were remarkably restrained by the increase of LINC00346. Moreover, we showed that LINC00346 overexpression activated the JAK‐STAT3 pathway, which is involved in many cancers. Afterward, in vivo experiments were utilized and we proved that LINC00346 was able to induce HCC tumor growth via activating the JAK‐STAT3 pathway. To conclude, we revealed the potential possibility of developing LINC00346 as an indicator for HCC.

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“…Similarly, in colon cancer, positive immunostaining rates for STAT3 and p-STAT3 were 72% (36/50) and 76% (38/50), respectively [58]. After reviewing 17 studies and a total of 2,346 colon cancer patients, the authors revealed a positive association between p-STAT3 expression and lymph node metastasis [59]. …”

Section: Leptin Biology and Molecules Of Relevant Signal Transductmentioning

confidence: 99%

The potential role of leptin in tumor invasion and metastasis

Ray

Cleary

2017

Cytokine & Growth Factor Reviews

110

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The adipocyte-released hormone-like cytokine/adipokine leptin behaves differently in obesity compared to its functions in the normal healthy state. In obese individuals, elevated leptin levels act as a pro-inflammatory adipokine and are associated with certain types of cancers. Further, a growing body of evidence suggests that higher circulating leptin concentrations and/or elevated expression of leptin receptors (Ob-R) in tumors may be poor prognostic factors. Although the underlying pathological mechanisms of leptin’s association with poor prognosis are not clear, leptin can impact the tumor microenvironment in several ways. For example, leptin is associated with a number of biological components that could lead to tumor cell invasion and distant metastasis. This includes interactions with carcinoma-associated fibroblasts, tumor promoting effects of infiltrating macrophages, activation of matrix metalloproteinases, transforming growth factor-β signaling, etc. Recent studies also have shown that leptin plays a role in the epithelial-mesenchymal transition, an important phenomenon for cancer cell migration and/or metastasis. Furthermore, leptin’s potentiating effects on insulin-like growth factor-I, epidermal growth factor receptor and HER2/neu have been reported. Regarding unfavorable prognosis, leptin has been shown to influence both adenocarcinomas and squamous cell carcinomas. Features of poor prognosis such as tumor invasion, lymph node involvement and distant metastasis have been recorded in several cancer types with higher levels of leptin and/or Ob-R. This review will describe the current scenario in a precise manner. In general, obesity indicates poor prognosis in cancer patients.

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The Role of p-STAT3 as a Prognostic and Clinicopathological Marker in Colorectal Cancer: A Systematic Review and Meta-Analysis

Cited by 43 publications

References 43 publications

Mesenchymal Stem Cell Administration Attenuates Colon Cancer Progression by Modulating the Immune Component within the Colorectal Tumor Microenvironment

Mesenchymal Stem Cell Administration Attenuates Colon Cancer Progression by Modulating the Immune Component within the Colorectal Tumor Microenvironment

LINC00346 promotes hepatocellular carcinoma progression via activating the JAK‐STAT3 signaling pathway

The potential role of leptin in tumor invasion and metastasis

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