The combined expression of Semaphorin4D and PlexinB1 predicts disease recurrence in colorectal cancer

Ikeya, Takashi; Maeda, Kiyoshi; Nagahara, Hisashi; Shibutani, Masatsune; Iseki, Yasuhito; Hirakawa, Kosei

doi:10.1186/s12885-016-2577-6

Cited by 19 publications

(19 citation statements)

References 18 publications

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“…All markers were found to be downregulated in recurrent tumors as compared to the breast tissues of disease-free patients. This contrasted with a recently published study defining the Sema4D and Plexin B1 expression levels in colorectal cancer, where increased expression of these molecules was found to be associated with a poorer prognosis (Ikeya et al, 2016 ). The Sema4D-Plexin B1 expression was found to be significantly related to tumor’s stage, depth of tumor invasion, lymph node metastasis, lymphatic invasion, and venous invasion, but unrelated to the patient’s age and gender.…”

Section: Introductioncontrasting

confidence: 76%

Neuroimmune semaphorins as costimulatory molecules and beyond

Chapoval

2018

Mol Med

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Several neuronal guidance proteins, known as semaphorin molecules, function in the immune system. This dual tissue performance has led to them being defined as “neuroimmune semaphorins”. They have been shown to regulate T cell activation by serving as costimulatory molecules. Similar to classical costimulatory molecules, neuroimmune semaphorins are either constitutively or inducibly expressed on immune cells. In contrast to the classical costimulatory molecule function, the action of neuroimmune semaphorins requires the presence of two signals, the first one provided by TCR/MHC engagement, and the second one provided by B7/CD28 interaction. Thus, neuroimmune semaphorins serve as a “signal three” for immune cell activation and regulate the overall intensity of immune response. The current knowledge on their structures, multiple receptors, specific cell/tissue/organ expression, and distinct functions in different diseases are summarized and discussed in this review.

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Section: Introductioncontrasting

confidence: 76%

Neuroimmune semaphorins as costimulatory molecules and beyond

Chapoval

2018

Mol Med

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“…Semaphorins, a family of secreted, transmembrane, and membrane-tethered proteins, are overexpressed in many cancers. Semaphorin4D (Sema4D, also CD100), is commonly overexpressed in head and neck, breast, ovarian, lung, prostate, and colon cancers (25)(26)(27)(28)(29). Receptor (plexin-B1) binding promotes association with and activation of the Met receptor, driving tumor cell invasiveness (30).…”

Section: Nerve Recruitmentmentioning

confidence: 99%

Exosomal Induction of Tumor Innervation

Vermeer

2019

Cancer Research

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The na€ ve view of tumors as isolated islands of rogue cells has given way to a deeper understanding of cancer as being closer to a foreign organ. This "organ" contains immunologic, vascular, and neural connections to its host that provide not only mechanisms for disease progression but also opportunities for therapeutic intervention. The presence of nerves within tumor tissues has long been appreciated. However, a mechanistic understanding of how tumors recruit nerves has been slower to emerge. Tumor release of neurotrophic factors and axonal guidance molecules likely directs axons toward the tumor bed. Newly emerging data support a contribution of tumor-released exosomes in the induction of axonogenesis toward the tumor. Exosomes, small membrane-bound vesicles that carry a complex cargo (DNA, RNA, miRNA, lipids, and proteins), protect their cargo from the low pH of the tumor microenvironment. They also represent an efficient means of local and distal communication between the tumor and potentially innervating nerves. Likely, a combination of neurotrophins, guidance molecules, and exosomes work in concert to promote tumor innervation. As such, defining the critical components driving tumor innervation will identify new targets for intervention. Moreover, with a deepening understanding, tumor innervation may emerge as a new hallmark of cancer.

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“…As for SEMA4D, accumulating evidences illustrated it was a potent inducer of angiogenesis, and its overexpression was associated with tumor progression and poor prognosis in a variety of malignancies (9, 23, 24). A series of studies accomplished by Zhou and the colleagues explained the SEMA4D in combination with VEGF to promote cancer progression synergistically.…”

Section: Discussionmentioning

confidence: 99%

Atezolizumab and Bevacizumab Attenuate Cisplatin Resistant Ovarian Cancer Cells Progression Synergistically via Suppressing Epithelial-Mesenchymal Transition

Zhang

Chen

et al. 2019

Front. Immunol.

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The AURELIA trial demonstrated that adding Bevacizumab to chemotherapy significantly improved progression-free survival (PFS) for platinum resistant recurrent ovarian cancer. Recently, immunotherapy also presented potential anti-tumor effects in several malignant solid tumors. This study aimed to investigate whether combining anti-PD-L1 Atezolizumab with BEV may have a synergistic effect and enhance the efficacy of both treatments in cisplatin resistant epithelial ovarian cancer (CREOC). We retrospectively analyzed 124 epithelial ovarian cancer (EOC) patients from Gynecologic Oncology Department of Tianjin Cancer Hospital between January 2013 and June 2018, who all were diagnosed with cisplatin resistance due to progressing <6 months after completing platinum-based therapy. Based on responding to at least 2 cycles of Bevacizumab-containing chemotherapy (BC), these Patients were divided into BC response group and BC non-response group. Immunohistochemistry was used to detect that PD-L1 expression and tumor angiogenesis-related proteins (VEGF and Semaphorin4D) in tissues from 124 patients with CREOC. The positive expressions of PD-L1, VEGF, and Semaphorin4D (SEMA4D) were found in 58.73, 50.79, and 71.43% of the 63 cases CREOC tissues with BC response, respectively, which were significantly higher than that in the 61 cases BC non-response group ( P < 0.05). PD-L1 expression correlated with SEMA4D and VEGF positively ( r = 0.344 and 0.363, P < 0.001). Over-expressions of PD-L1, VEGF and SEMA4D are associated with more malignant clinicopathologic characteristics of CREOC Patients. In survival analysis, patients' response to BC was the independent factor for evaluation of PFS and overall survival (OS). Cell functional assays showed that Atezolizumab in combination with Bevacizumab inhibited the proliferation, migration, and invasion of cisplatin resistant ovarian cancer cell line A2780cis in vitro synergistically, which maybe associate with Bevacizumab suppressing the epithelial-mesenchymal transition (EMT) and PD-L1 expression by targeting STAT3. Furthermore, Bevacizumab and Atezolizumab induced synergistic anti-tumor effect in vivo . These findings suggest a novel therapeutic strategy for cisplatin resistant recurrent EOC and its mechanism warrants further study.

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The combined expression of Semaphorin4D and PlexinB1 predicts disease recurrence in colorectal cancer

Cited by 19 publications

References 18 publications

Neuroimmune semaphorins as costimulatory molecules and beyond

Neuroimmune semaphorins as costimulatory molecules and beyond

Exosomal Induction of Tumor Innervation

Atezolizumab and Bevacizumab Attenuate Cisplatin Resistant Ovarian Cancer Cells Progression Synergistically via Suppressing Epithelial-Mesenchymal Transition

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