TM4SF1 as a prognostic marker of pancreatic ductal adenocarcinoma is involved in migration and invasion of cancer cells

Zheng, Biao; Ohuchida, Kenoki; Chen, Lin; Zhao, Ming; Shindo, Koji; Fujiwara, Kenji; Manabe, Tatsuya; Torata, Nobuhiro; Moriyama, Taiki; Miyasaka, Yoshihiro; Ohtsuka, Takao; Takahata, Shunichi; Mizumoto, Kazuhiro; Oda, Yoshinao; Tanaka, Masao

doi:10.3892/ijo.2015.3022

Cited by 24 publications

(29 citation statements)

References 37 publications

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“…The results suggested that TM4SF1 was a tumor suppressor in GC progression and invasion. Similar result was also obtained in the study that showed contribution of TM4SF1 loss to the invasion and migration of pancreatic cancer cells . However, other study showed that high expression of TM4SF1 is correlated with T stage, TNM stage, lymph node metastasis status of MIBC (muscle invasive bladder cancer) patients .…”

Section: Discussionsupporting

confidence: 86%

Clinical significance of TM4SF1 as a tumor suppressor gene in gastric cancer

et al. 2018

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Transmembrane‐4‐L‐six‐family member‐1 (TM4SF1), a tumor‐associated antigen, is overexpressed in most epithelial cell carcinomas and a potential target for antibody‐mediated therapy. However, the role of TM4SF1 in gastric cancer has not been elucidated. The aim of this study was to investigate the clinical significance of TM4SF1 expression in gastric carcinoma (GC) tissues using 152 GC tissue samples and matched adjacent nontumor tissue samples analyzed by immunohistochemistry, and 13 fresh GC tissue samples analyzed by Western blotting. The results showed that TM4SF1 was heterogeneously expressed in normal gastric mucosa, with a high expression rate in fundus mucosa. Higher levels and strong expression rate of TM4SF1 were associated with GC tissues of higher‐grade differentiation. TM4SF1 levels were lower in gastric cancer tissues than gastric noncancerous tissues. Expression of TM4SF1 was not correlated with USP10 (P = 0.157), S100A12 (P = 0.479), p53 (P = 0.249), or Ki67 (P = 0.166) in GC. The expression of TM4SF1 was significantly and negatively correlated with depth of invasion (P = 0.031), nodal metastasis (P = 0.042), TNM stage (P = 0.030), and Lauren classification (P = 0.026). There was no significant correlation between TM4SF1 expression and age, gender, tumor size, or distant metastasis (P > 0.05). The expression of TM4SF1 was associated with well overall survival (P = 0.0164). The 5‐year survival rate for patients with GC showing TM4SF1 positive was 58.82% (10/17), and the median survival time was 78 months, higher than that (12.90%, 12/93) of patients who were TM4SF1 negative, whose median survival time was 62 months. These data suggested that low expression of TM4SF1 is associated with carcinogenesis and development, tumor progression and invasion of gastric cancer, and poor overall survival of patients with GC. TM4SF1 is a tumor suppressor for GC and a novel prognostic marker for patients with GC.

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Section: Discussionsupporting

confidence: 86%

Clinical significance of TM4SF1 as a tumor suppressor gene in gastric cancer

et al. 2018

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“…Upregulated expression of TM4SF1 in lung cancer cells significantly increased their invasiveness in vitro and significantly decreased the survival time of xenograft mice, whereas silencing of TM4SF1 greatly inhibited tumor cell migration and invasion (Kao et al, 2003). Another study showed that decreased TM4SF1 expression enhanced the migration and invasion of pancreatic tumor cells in vitro (Zheng B. et al, 2015). In addition, silencing of TM4SF1 decreased the odds of lung and liver metastases in orthotopic pancreatic cancer (Cao et al, 2016).…”

Section: Tm4sf1 Promotes Cancer Proliferation and Migrationmentioning

confidence: 96%

“…Higher level expression of TM4SF1 was involved in GC tissues of higher grade differentiation. In addition, Zheng B. et al (2015) reported that patients with high levels of TM4SF1 showed longer survival time than those with low TM4SF1 levels. In vitro, reduced TM4SF1 expression after TGF-ß1-induced EMT enhanced the migration and invasion of pancreatic cancer cells partially via decreased E-cadherin expression.…”

Section: Clinical Prognosis Of Tm4sf1 Expressionmentioning

confidence: 99%

Role of Transmembrane 4 L Six Family 1 in the Development and Progression of Cancer

Yang²,

Zheng

et al. 2020

Front. Mol. Biosci.

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Transmembrane 4 L six family 1 (TM4SF1) is a protein with four transmembrane domains that belongs to the transmembrane 4 L six family members (TM4SFs). Structurally, TM4SF1 consists of four transmembrane domains (TM1-4), N-and C-terminal intracellular domains, two extracellular domains, a smaller domain between TM1 and TM2, and a larger domain between TM3 and TM4. Within the cell, TM4SF1 is located at the cell surface where it transmits extracellular signals into the cytoplasm. TM4SF1 interacts with tetraspanins, integrin, receptor tyrosine kinases, and other proteins to form tetraspanin-enriched microdomains. This interaction affects the pro-migratory activity of the cells, and thus it plays important roles in the development and progression of cancer. TM4SF1 has been shown to be overexpressed in many malignant tumors, including gliomas; malignant melanomas; and liver, prostate, breast, pancreatic, bladder, colon, lung, gastric, ovarian, and thyroid cancers. TM4SF1 promotes the migration and invasion of cancer cells by inducing epithelial-mesenchymal transition, self-renewal ability, tumor angiogenesis, invadopodia formation, and regulating the related signaling pathway. TM4SF1 is an independent prognostic indicator and biomarker in several cancers. It also promotes drug resistance, which is a major cause of therapeutic failure. These characteristics make TM4SF1 an attractive target for antibody-based immunotherapy. Here, we review the many functions of TM4SF1 in malignant tumors, with the aim to understand the interaction between its expression and the biological behaviors of cancer and to supply a basis for exploring new therapeutic targets.

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“…TM4SF1 has been reported to be associated with many tumors invasion and metastasis [38, 39], but has not been reported in esophageal cancer. The results presented in this study showed that TM4SF1 overexpression significantly enhanced KYSE150 and KYSE180 cells invasion and migration.…”

Section: Discussionmentioning

confidence: 99%

TM4SF1 promotes the self-renewal of esophageal cancer stem-like cells and is regulated by miR-141

Xue

Jiang

et al. 2016

Oncotarget

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Cancer stem-like cells have been identified in primary human tumors and cancer cell lines. Previously we found TM4SF1 gene was highly expressed in side population (SP) cells from esophageal squamous cell carcinoma (ESCC) cell lines, but the role and underlying mechanism of TM4SF1 in ESCC remain unclear. In this study, we observed TM4SF1 was up-regulated but miR-141 was down-regulated in SP cells isolated from ESCC cell lines. TM4SF1 could stimulate the self-renewal ability and carcinogenicity of esophageal cancer stem-like cells, and promote cell invasion and migration. In miR-141 overexpression cells, the expression of TM4SF1 was significantly reduced. We also found that overexpression of miR-141 could abolish the self-renewal ability and carcinogenicity of esophageal cancer stem-like cells and decrease cell invasion and migration by suppressing TM4SF1. Consequently, TM4SF1 is a direct target gene of miR-141. The regulation of TM4SF1 by miR-141 may play an important role in controlling self-renewals of esophageal cancer stem-like cells. It may also promote the development of new therapeutic strategies and efficient drugs to target ESCC stem-like cells.

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TM4SF1 as a prognostic marker of pancreatic ductal adenocarcinoma is involved in migration and invasion of cancer cells

Cited by 24 publications

References 37 publications

Clinical significance of TM4SF1 as a tumor suppressor gene in gastric cancer

Clinical significance of TM4SF1 as a tumor suppressor gene in gastric cancer

Role of Transmembrane 4 L Six Family 1 in the Development and Progression of Cancer

TM4SF1 promotes the self-renewal of esophageal cancer stem-like cells and is regulated by miR-141

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