Exosome-transmitted lncRNA PCGEM1 promotes invasive and metastasis in gastric cancer by maintaining the stability of SNAI1

Piao, Haiyan; Guo, Shu; Wang, Y.; Zhang, Jun

doi:10.1007/s12094-020-02412-9

Cited by 46 publications

(33 citation statements)

References 30 publications

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“…The hypoxia-responsive involvement of lncRNAs [ 273 , 328 , 329 ] and circRNAs [ 330 , 331 ] in the mechanisms of EMT and cancer stemness can also be interpreted as a contribution of these epigenetic regulators to the radioresistance of hypoxic tumors, since CSC-like cells generated in hypoxic niches are radioresistant and also have an ability to form distant metastases, thus becoming unavailable for radiotherapeutic exposure by being focused on the primary tumor (see Section 7.1 and Figure 2 ).…”

Section: How Do Epigenetic Regulators Affect the Radioresistance Omentioning

confidence: 99%

“…In another model, exosomes secreted by hypoxic hepatocellular carcinoma cells promoted EMT and metastases by transferring miR-1273f, which activated the Wnt/β-catenin pathway in the recipient cancer cells [ 323 ]. As for exosomal long noncoding RNAs, the hypoxia-induced transmission of exosomal lncRNA PCGEM1 was found to promote cell migration, invasiveness and metastatic potential in gastric cancer cells by maintaining the stability of SNAI1, which induced EMT [ 329 ].…”

Section: Hypoxia-induced Exosome Generation By Tumor Cellsmentioning

confidence: 99%

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Hypoxia-Induced Cancer Cell Responses Driving Radioresistance of Hypoxic Tumors: Approaches to Targeting and Radiosensitizing

Kabakov

Yakimova

2021

Cancers

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Within aggressive malignancies, there usually are the “hypoxic zones”—poorly vascularized regions where tumor cells undergo oxygen deficiency through inadequate blood supply. Besides, hypoxia may arise in tumors as a result of antiangiogenic therapy or transarterial embolization. Adapting to hypoxia, tumor cells acquire a hypoxia-resistant phenotype with the characteristic alterations in signaling, gene expression and metabolism. Both the lack of oxygen by itself and the hypoxia-responsive phenotypic modulations render tumor cells more radioresistant, so that hypoxic tumors are a serious challenge for radiotherapy. An understanding of causes of the radioresistance of hypoxic tumors would help to develop novel ways for overcoming this challenge. Molecular targets for and various approaches to radiosensitizing hypoxic tumors are considered in the present review. It is here analyzed how the hypoxia-induced cellular responses involving hypoxia-inducible factor-1, heat shock transcription factor 1, heat shock proteins, glucose-regulated proteins, epigenetic regulators, autophagy, energy metabolism reprogramming, epithelial–mesenchymal transition and exosome generation contribute to the radioresistance of hypoxic tumors or may be inhibited for attenuating this radioresistance. The pretreatments with a multitarget inhibition of the cancer cell adaptation to hypoxia seem to be a promising approach to sensitizing hypoxic carcinomas, gliomas, lymphomas, sarcomas to radiotherapy and, also, liver tumors to radioembolization.

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Section: How Do Epigenetic Regulators Affect the Radioresistance Omentioning

confidence: 99%

Section: Hypoxia-induced Exosome Generation By Tumor Cellsmentioning

confidence: 99%

Hypoxia-Induced Cancer Cell Responses Driving Radioresistance of Hypoxic Tumors: Approaches to Targeting and Radiosensitizing

Kabakov

Yakimova

2021

Cancers

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“…Epithelial-mesenchymal transition (EMT) is a biological process associated with increased cell motility, resistance to apoptosis and senescence, and suppressed immune reaction during the initial step of metastasis ( 29 ) and is closely regulated by TDEs ( 30 ). LncRNA ZFAS1 and PCGEM1 are highly enriched in gastric cancer TDEs and are capable of inducing EMT phenotypes among cancer cells during metastasis, in which PCGEM1 stabilizes SNAI1 ( 31 , 32 ). CircNRIP1, a circular RNA, can also be transmitted among gastric cancer cells through exosomes and regulate EMT through a circNRIP1-miR-149-5p-AKT1/mTOR axis ( 33 ).…”

Section: Roles Of Exosomes In Gastric Cancer Malignitymentioning

confidence: 99%

Exosomes Promote Pre-Metastatic Niche Formation in Gastric Cancer

Gao

Song

et al. 2021

Front. Oncol.

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Gastric cancer has a high rate of metastasis, during which pre-metastatic niches (PMN) provide a supportive environment for the upcoming tumor cells. Exosomes are bilayer vesicles secreted by cells containing biological information that mediates communication between cells. Using exosomes, gastric cancer cells establish PMN remotely in multifarious perspectives, including immunosuppression, stroma remodeling, angiogenesis, mesothelial mesenchymal transformation, and organotropism. In turn, the cell components in PMN secrete exosomes that interact with each other and provide onco-promoting signals. In this review, we highlight the role of exosomes in PMN formation in gastric cancer and discuss their potential values in gastric cancer metastasis diagnosis, prevention, and treatment.

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“…The exosomal lncRNA PCGEM1 promoted invasion and metastasis of GC by stabilizing SNAIL. 26 Exosomal lncRNA CEBPA-AS1 secreted by GC cells could promote cell proliferation, inhibiting apoptosis and induces GC progression. 27 Exosomal lncRNA metastasis-associated lung adenocancer transcript 1 (MALAT-1) sponging miR-26a/26b promoted the invasion and metastasis of CRC by regulating FUT4 and activating the PI3K/Akt/mTOR pathway.…”

Section: The Molecular Mechanism Of Exosomal Lncrnas In Cancersmentioning

confidence: 99%