Cancer‐associated fibroblasts–derived exosomes‐mediated transfer of LINC00355 regulates bladder cancer cell proliferation and invasion

Yan, Lei; Wang, Peiyu; Fang, Wen-Liang; Liang, Chaozhao

doi:10.1002/cbf.3462

Cited by 47 publications

(31 citation statements)

References 27 publications

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“…Our data are consistent with the newly recent reports about LINC00355 acting as an oncogene in other cancers, including bladder cancer, head and neck squamous cell carcinoma, and lung adenocarcinoma [43][44][45] .…”

Section: Discussionsupporting

confidence: 93%

RETRACTED ARTICLE: LINC00355 induces gastric cancer proliferation and invasion through promoting ubiquitination of P53

Zhao

Jin

et al. 2020

Cell Death Discov.

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Long noncoding RNAs (LncRNAs) have been reported to play critical roles in gastric cancer, but true biomarkers remain unknown. In this study, we found a new lncRNA LINC00355 that was involved in malignant progression of gastric cancer (GC) and further revealed its role and mechanism. Differentially expressed lncRNAs were identified through bioinformatics, and qRT-PCR was used to validate the expression of LINC00355 in gastric cancer tissues and cells. The biological role of LINC00355 in GC was detected by gene overexpression and knockdown experiments. Subcellular fractionation, qRT-PCR, and FISH were performed to detect the subcellular localization. Co-IP and western blotting were used to study the ubiquitination-mediated regulation of P53 and the expression of the E3 ligases RAD18 and UBE3C. The results showed that LINC00355 was significantly increased in gastric cancer cell lines and patient tissues and closely correlated with late stages, distant metastasis, and poor prognosis of patients. High expression of LINC00355 promoted the proliferation and invasion of gastric cancer cells in vivo and in vitro. Mechanistic studies found that LINC00355 that mainly located in the nucleus, acting as a transcriptional activator, promoted transcription of RAD18 and UBE3C, which both bind to P53 and mediate the ubiquitination and degradation of P53. Furthermore, LINC00355 overexpression enhanced the ubiquitination process, and LINC00355 knockdown alleviated it. These results indicated that LINC00355 induces gastric cancer cell proliferation and invasion by promoting transcription of RAD18 and UBE3C, which mediates ubiquitination of P53 and thereby plays a critical role in survival and tumorigenicity of gastric cancer cells. LINC00355 may represent a new mechanism for GC progression and provide a potential marker for GC diagnosis and treatment.

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Section: Discussionsupporting

confidence: 93%

RETRACTED ARTICLE: LINC00355 induces gastric cancer proliferation and invasion through promoting ubiquitination of P53

Zhao

Jin

et al. 2020

Cell Death Discov.

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“…We found that the CDC25C/CDK1/RRM2-LINC00355 ceRNA relationship can affect non-small cell lung cancer. It is reported in recent studies that exosomes-mediated LINC00355 regulates bladder cancer cell proliferation and invasion [ 38 ]. Identification of these markers will further improve understanding of lncRNA-mediated pathway regulation and ceRNA functions.…”

Section: Discussionmentioning

confidence: 99%

Prediction of Specific Subtypes and Common Markers of Non-Small Cell Lung Cancer Based on Competing Endogenous RNA Network

Liu

Wang²,

Yang

et al. 2020

Med Sci Monit

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Background There are various pathological types of lung cancer, including squamous cell carcinoma and adenocarcinoma. Although both of them are lung cancers, there are significant differences in diagnosis, pathogenesis, location, imaging, metastasis, and treatment. According to the competing endogenous RNA (ceRNA) theory, long non-coding RNAs (lncRNAs) compete with encoding protein genes (mRNAs) to connect with miRNAs, thus affecting the level of mRNA. Material/Methods First, using the t test, we identified mRNAs and lncRNAs that have different expressions (fold change >2, P<0.01) in normal samples and in tumor samples. We calculated the significance of the shared miRNAs for mRNAs and lncRNAs by hypergeometric test (P<0.01). Further, mRNA and lncRNA pairs with co-expression relationships in cancer samples were used to establish ceRNA networks. Then, the random walk algorithm was used to optimize the specific ceRNA networks and identify potential prognostic markers of survival. Finally, we built a common ceRNA network to find markers of non-small-cell lung cancer. Results We identified some potential key markers, such as PVT1, LINC00472, CDKN2A, and FAM83B, in LUSC and HOXA11-AS, HNF1A-AS1, LINC00511, and HOTAIR in LUAD by analyzing the ceRNA networks. Moreover, a number of common ceRNA pairs, such as CDC25C/CDK1/RRM2-LINC00355, have been found, and they are also significant markers for tumor survival and prognosis. Conclusions In summary, the present study provides a comparative analysis in 2 kinds of lung cancer ceRNA networks. Some specific and common markers we predicted that may be of great importance for clinical diagnosis and treatment.

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“…A study of exosomes secreted from cancer cells showed stimulation of fibroblasts into myofibroblast through tumor growth factor (TGF)-β , thereby contributing to tumor progression 28 . In another study, the increase in LINC00355 expression of CAFs promoted the proliferation and invasiveness of bladder cancer 29 . In a study of ovarian cancer, it was found that exosomes from ovarian cancer cells affected fibroblast cells of tumor origin and cells adjacent to the tumor 30 .…”

Section: Effect Of Cdes On Cafsmentioning

confidence: 90%

Concise review: The role of cancer-derived exosomes in tumorigenesis and immune cell modulation

2020

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Exosomes are subcellular entities which were first discovered in the 1980s. Over the past decade, scientists have discovered that they carry components of genetic information that allow for cell-cell communication and cell targeting. Exosomes secreted by cancer cells are termed cancer-derived exosomes (CDEs), and play an important role in tumor formation and progression. Specifically, CDEs mediate the communication between cancer cells, as well as between cancer cells and other cells in the tumor microenvironment, including cancer-associated fibroblasts, endothelial cells, mesenchymal stem cells, and effector immune cells. Additionally, through the vascular system and body fluids, CDEs can modulate response to drugs, increase angiogenesis, stimulate proliferation, promote invasion and metastasis, and facilitate escape from immune surveillance. This review will discuss the relationship between cancer cells and other cells (particularly immune cells), as mediated through CDEs, as well as the subsequent impact on tumorigenesis and immunomodulation. Understanding the role of CDEs in tumorigenesis and immune cell modulation will help advance their utilization in the diagnosis, prognosis, and treatment of cancer.

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Cancer‐associated fibroblasts–derived exosomes‐mediated transfer of LINC00355 regulates bladder cancer cell proliferation and invasion

Cited by 47 publications

References 27 publications

RETRACTED ARTICLE: LINC00355 induces gastric cancer proliferation and invasion through promoting ubiquitination of P53

RETRACTED ARTICLE: LINC00355 induces gastric cancer proliferation and invasion through promoting ubiquitination of P53

Prediction of Specific Subtypes and Common Markers of Non-Small Cell Lung Cancer Based on Competing Endogenous RNA Network

Concise review: The role of cancer-derived exosomes in tumorigenesis and immune cell modulation

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