Gastric cancer: Basic aspects

Molina-Castro, Silvia; Pereira-Marques, Joana; Figueiredo, Céu; Machado, José Carlos; Varon, Christine

doi:10.1111/hel.12412

Cited by 38 publications

(34 citation statements)

References 60 publications

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“…Additionally, it has been found that the incidence of GC is twice as high in men than in women, implying that hormonal differences may also be risk factors for GC progression [ 10 , 11 ]. In recent years, with the development of enteroscopy and surgical techniques, the five-year overall survival rate for early-stage GC patients has significantly improved, but for advanced-stage GC patients, the five-year survival rate is still unsatisfactory at <25% [ 12 , 13 ]. The high mortality of GC is mainly attributed to delayed diagnosis due to the absence of screening programs; the lack of desirable molecular biomarkers and the paucity of specific early clinical symptoms; and the common forms of recurrence, including peritoneal dissemination, hematogenous spread, and lymph node metastasis [ 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNAs: New Regulators of Resistance to Systemic Therapies for Gastric Cancer

Sun

Jiang

et al. 2021

BioMed Research International

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Gastric cancer (GC) is the second leading cause of cancer mortality and the fourth most commonly diagnosed malignant disease, with approximately 951,000 new cases diagnosed and approximately 723,000 cases of mortality each year. The highest mortality rate of GC is in East Asia, and the lowest is in North America. A large number of studies have demonstrated that GC patients are characterized by higher morbidity, metastasis rates, and mortality and lower early diagnosis rates, radical resection rates, and 5-year survival rates. All cases of GC can be divided into two important stages, namely, early- and advanced-stage GC, and the stage mainly determines the treatment strategy for and the therapeutic effect in GC patients. Patients with early-stage GC undergo radical surgery followed by chemotherapy, and the 5-year survival rate can be as high as 90%. However, patients with advanced-stage GC cannot undergo radical surgery because they are at risk for metastasis; therefore, they can choose only radiotherapy or chemotherapy and have a poor prognosis. Based on the lack of specific clinical manifestations and detection methods, most GC patients (>70%) are diagnosed in the advanced stage; therefore, continued efforts toward developing treatments have been focused on advanced-stage GC patients and include molecular targeted therapy, immunotherapy, and small molecular therapy. Nevertheless, in recent years, accumulating evidence has indicated that small molecules, especially long noncoding RNAs (lncRNAs), are involved in the occurrence, development, and progression of GC, and their abundantly dysregulated expression has been identified in GC tissues and cell lines. Therefore, lncRNAs are considered easily detectable molecules and ideal biomarkers or target-specific agents for the future diagnosis or treatment of GC. In this review, we primarily discuss the status of GC, the role of lncRNAs in GC, and the emerging systemic treatments for GC.

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Section: Introductionmentioning

confidence: 99%

Long Noncoding RNAs: New Regulators of Resistance to Systemic Therapies for Gastric Cancer

Sun

Jiang

et al. 2021

BioMed Research International

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“…It is reported that EpCAM(+)/CD44(+) cells grow exponentially in vitro as cancer spheres in SFM [25]. Furthermore, pluripotent stem cell factors like Oct4, Sox2 and Nanog also regulate GCSCs properties [13,26]. In the present study, we showed signi cantly elevated tumorsphere formation capacity of both BGC-823 and SGC-7901 cells cultured in SFM, as well as markedly increased expression levels of GCSCs markers in the sphere-forming cells, which depicted the enrichment of GCSCs.…”

Section: Discussionmentioning

confidence: 99%

“…GCSCs were rst described in 2007 by Yang et al [12]. Accumulating evidence indicates that GCSCs are the root of gastric cancer development and progression [13][14][15][16][17]. Moreover, chemotherapy has been found to induce cancer cell stemness [18].…”

Section: Introductionmentioning

confidence: 99%

Apatinib Suppresses Gastric Cancer Stem Cells Properties by Inhibiting Sonic Hedgehog Pathway

Cao

Sun

et al. 2020

Preprint

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Background Gastric cancer stem cells (GCSCs) are considered as the basis of gastric carcinoma onset. Sonic Hedgehog (SHH) pathway plays a crucial role in maintaining GCSCs characteristics. Apatinib, a highly selective vascular endothelial growth factor receptor 2 (VEGFR-2) inhibitor, has been approved in China for the treatment of advanced gastric cancer after the failure of second-line therapy. To data, the effects of apatinib on GCSCs and the underlying mechanisms have not been elucidated yet.Methods Tumorsphere formation assay was used to enrich GCSCs from BGC-823 and SGC-7901 cells and the number of CD133-positive cells was examined by flow cytometry. Western blotting, immunofluorescence and immunohistochemistry assays were used to determine protein expression. Cell proliferation and apoptosis of GCSCs after apatinib treatment were evaluated by CCK8, colony formation, flow cytometry and Hoechst 33258 assays. Transient transfection assay was used to upregulate Gli1 expression in GCSCs. Nude mouse xenograft was used to investigate the suppressive effects of apatinib in vivo. Results We revealed that the levels of GCSCs markers and the number of CD133-positive cells were significantly elevated in the sphere-forming cells. We further illustrated that apatinib efficiently abolished GCSCs traits, as manifested by inhibition of tumorsphere formation, decreased expression of GCSCs markers, reduced number of CD133-positive cells, drug resistance protein suppression as well as proliferation inhibition and apoptosis induction. Furthermore, we found that apatinib downregulated the activation of SHH pathway, while upregulation of SHH pathway attenuated the inhibitory effects of apatinib on GCSCs. Furthermore, apatinib treatment significantly delayed tumor growth and inhibited GCSCs characteristics in xenograft model. Conclusions Taken together, our data suggested that apatinib exhibited its inhibitory effects on GCSCs via suppression of SHH pathway. These findings could provide new insights into the therapeutic application of apatinib in GCSCs suppression and advanced gastric cancer treatment.

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“…Although the incidence of gastric cancer has decreased in recent years (1,2), it remains the third leading cause of cancer-associated mortality worldwide, with ~1,000,000 new cases diagnosed each year (3,4). Improved techniques for the treatment of gastric cancer have been developed, including novel surgical methods, radiation and chemotherapy protocols; however, the prognoses of patients with advanced gastric cancer remain poor, with a 5-year survival of 5–20% (5,6).…”

Section: Introductionmentioning

confidence: 99%

Tanshinone IIA inhibits cell proliferation and tumor growth by downregulating STAT3 in human gastric cancer

et al. 2018

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Gastric cancer is the third leading cause of cancer-associated deaths worldwide. Research into the underlying mechanisms of gastric cancer is essential for the development of novel therapeutic agents to improve the prognoses of patients with gastric cancer. Tanshinone IIA (Tan IIA) is the pure extract of Danshen root (Salvia miltiorrhiza) and has been report to inhibit the proliferation of gastric cancer cells; however, the intrinsic underlying mechanisms remain unclear. The aim of the present study was to investigate whether Tan IIA has a direct anti-cancer effect in gastric cancer cells and determine the underlying mechanisms responsible. The results revealed that Tan IIA effectively inhibits proliferation in three human gastric cancer cell lines (SNU-638, MKN1 and AGS) in a time- and dose-dependent manner. Furthermore, Tan IIA treatment induced an increase in apoptosis, B-cell lymphoma (Bcl-2)-associated protein X expression and cleaved caspase-3 levels, as well as a decrease in Bcl-2 expression. Treatment with Tan IIA inhibited Furthermore, treatment with Tan IIA significantly inhibited the phosphorylation of signal transducer and activator of transcription 3 (STAT3), which may be responsible for the changes in apoptosis gene expression. However, overexpression of STAT3 significantly ameliorated the Tan IIA-induced suppression of cell growth and apoptosis. A nude mouse xenograft model was constructed and the results revealed that intraperitoneal Tan IIA treatment for 28 days significantly inhibited tumor growth and STAT3 activation. The results of the present study suggest that Tan IIA exerts potent anti-cancer activity in gastric cancer cells and this effect is mediated by the downregulation of STAT3 activation.

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Gastric cancer: Basic aspects

Cited by 38 publications

References 60 publications

Long Noncoding RNAs: New Regulators of Resistance to Systemic Therapies for Gastric Cancer

Long Noncoding RNAs: New Regulators of Resistance to Systemic Therapies for Gastric Cancer

Apatinib Suppresses Gastric Cancer Stem Cells Properties by Inhibiting Sonic Hedgehog Pathway

Tanshinone IIA inhibits cell proliferation and tumor growth by downregulating STAT3 in human gastric cancer

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