LncRNA EPIC1 promotes proliferation and inhibits apoptosis of gallbladder cancer cells by interacting with LET

Fu, Changbo; Yin, Tao; Xu, Xuan; Lu, Weijun

doi:10.1016/j.aohep.2021.100563

Cited by 7 publications

(4 citation statements)

References 15 publications

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“…In silico analysis revealed minor coding potential of the 545 nucleotides long TMEM244 transcript. TMEM244 has an open reading frame (ORF) but, as shown for other lncRNAs, such as LINC00116 or LINC00948, possessing an ORF does not determine protein production [ 15 , 16 ]. TMEM244 , like lncRNAs, is poorly conserved and its expression level is lower compared to protein-coding genes [ 17 ].…”

Section: Discussionmentioning

confidence: 99%

“…Recently, emerging evidence showed that lncRNAs could promote cell proliferation and, therefore, be engaged in carcinogenesis. For instance, the lncRNA HOXD cluster antisense RNA 1 ( HOXD-AS1 ) was upregulated and promoted cell proliferation in cervical cancer, while lncRNA EPIC1 promoted proliferation and inhibited apoptosis of gallbladder cancer cells [ 16 , 20 ]. LncRNAs can also affect apoptosis by acting as a competitive endogenous RNA (ceRNA) for miRNA and binding to the sequence at the 5′ end of the miRNA, therefore reducing target mRNA expression and ultimately affecting cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…LncRNAs can also affect apoptosis by acting as a competitive endogenous RNA (ceRNA) for miRNA and binding to the sequence at the 5′ end of the miRNA, therefore reducing target mRNA expression and ultimately affecting cell apoptosis. Moreover, lncRNAs can act directly or indirectly on death receptors [ 16 ]. Previous studies have demonstrated that in some cases, a non-protein-coding locus can give rise to functionally distinct transcript isoforms [ 21 , 22 , 23 , 24 ].…”

Section: Discussionmentioning

confidence: 99%

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TMEM244 Is a Long Non-Coding RNA Necessary for CTCL Cell Growth

Rassek

Iżykowska

Żurawek

et al. 2023

IJMS

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Transmembrane protein 244 (TMEM244) was annotated to be a member of the TMEM family, which are is a component of cell membranes and is involved in many cellular processes. To date, the expression of the TMEM244 protein has not been experimentally confirmed, and its function has not been clarified. Recently, the expression of the TMEM244 gene was acknowledged to be a diagnostic marker for Sézary syndrome, a rare cutaneous T-cell lymphoma (CTCL). In this study, we aimed to determine the role of the TMEM244 gene in CTCL cells. Two CTCL cell lines were transfected with shRNAs targeting the TMEM244 transcript. The phenotypic effect of TMEM244 knockdown was validated using green fluorescent protein (GFP) growth competition assays and AnnexinV/7AAD staining. Western blot analysis was performed to identify the TMEM244 protein. Our results indicate that TMEM244 is not a protein-coding gene but a long non-coding RNA (lncRNA) that is necessary for the growth of CTCL cells.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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TMEM244 Is a Long Non-Coding RNA Necessary for CTCL Cell Growth

Rassek

Iżykowska

Żurawek

et al. 2023

IJMS

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“…Gallbladder cancer (GBC) is the high malignancy of the biliary tract system which is caused by the imbalance of oxidation-reduction, and it influences more than 210,000 people and causes over 160,000 deaths every year (Su et al, 2021). The limited outcomes for GBC often results from late diagnosis, and then the 5-year survival rate is still low (C. Fu et al, 2021). During the early stage of GBC, most patients are asymptomatic (Zhu et al, 2021).…”

Section: Introductionmentioning

confidence: 99%

Knockdown of IGF2BP3 inhibits the tumorigenesis of gallbladder cancer and modifies tumor microenvironment

Qin

Zhang

Lei

et al. 2022

Drug Development Research

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Gallbladder cancer (GBC) ranks seventh among the gastrointestinal cancers. Messenger RNAs (mRNAs) could regulate the progression of GBC. For the purpose of exploring the targets for GBC treatment, RNA sequencing was used to identify the differential expressed mRNAs between GBC and adjacent tissues. Next, CCK8 assay was used to assess the cell viability, and cell proliferation was investigated by colony formation assay. Flow cytometry was performed to evaluate the cell apoptosis. Protein and mRNA expression were analyzed by western blot and RT‐qPCR, respectively. Transwell was performed to evaluate the cell metastasis. GBC‐derived exosomes were isolated with ultracentrifugation. To evaluate the function of exosomes in GBC, in vivo model of GBC was constructed. The data revealed IGF2BP3 was identified to be upregulated in GBC, and IGF2BP3 silencing was able to decrease GBC cell proliferation by promoting the apoptosis. The migration and invasion of GBC cells were reduced by IGF2BP3 knockdown. Silencing of IGF2BP3 obviously suppressed the level of p‐STAT3 in GBC cells. Meanwhile, GBC cell‐derived exosomes notably promoted macrophage M2 polarization via carrying IGF2BP3, and then the polarized macrophages promoted the malignant behavior of GBC cells. Furthermore, exosomes markedly promoted the tumor growth of GBC via promoting macrophage M2 polarization. In summary, knockdown of IGF2BP3 suppressed the malignant behavior of GBC cells. Additionally, knockdown of IGF2BP3 modified tumor microenvironment during the progression of GBC. Thus, these findings might provide a new theoretical basis for exploring a strategies against GBC.

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