A new long noncoding RNA (lncRNA) is induced in cutaneous squamous cell carcinoma and down-regulates several anticancer and cell differentiation genes in mouse

Ponzio, Gilles; Rezzonico, Roger; Bourget, Isabelle; Allan, Richard; Nottet, Nicolas; Popa, Alexandra; Magnone, Virginie; Rios, Géraldine; Mari, Bernard; Barbry, Pascal

doi:10.1074/jbc.m117.776260

Cited by 30 publications

(29 citation statements)

References 62 publications

(63 reference statements)

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“…BASP1 is also downregulated in lung cancer by specific miR‐191‐mediated mRNA degradation (Xu et al , ). In mouse, BASP1 is downregulated among several other anticancer genes in induced cutaneous squamous cell carcinoma by the long noncoding RNA AK144841 (Ponzio et al , ). Recently, tumor‐suppressive functions of BASP1 have been observed in several human cancer cell types.…”

Section: Introductionmentioning

confidence: 99%

The brain acid‐soluble protein 1 (BASP1) interferes with the oncogenic capacity of MYC and its binding to calmodulin

et al. 2020

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The MYC protein is a transcription factor with oncogenic potential controlling fundamental cellular processes such as cell proliferation, metabolism, differentiation, and apoptosis. The MYC gene is a major cancer driver, and elevated MYC protein levels are a hallmark of most human cancers. We have previously shown that the brain acid‐soluble protein 1 gene (BASP1) is specifically downregulated by the v‐myc oncogene and that ectopic BASP1 expression inhibits v‐myc‐induced cell transformation. The 11‐amino acid effector domain of the BASP1 protein interacts with the calcium sensor calmodulin (CaM) and is mainly responsible for this inhibitory function. We also reported recently that CaM interacts with all MYC variant proteins and that ectopic CaM increases the transactivation and transformation potential of the v‐Myc protein. Here, we show that the presence of excess BASP1 or of a synthetic BASP1 effector domain peptide leads to displacement of v‐Myc from CaM. The protein stability of v‐Myc is decreased in cells co‐expressing v‐Myc and BASP1, which may account for the inhibition of v‐Myc. Furthermore, suppression of v‐Myc‐triggered transcriptional activation and cell transformation is compensated by ectopic CaM, suggesting that BASP1‐mediated withdrawal of CaM from v‐Myc is a crucial event in the inhibition. In view of the tumor‐suppressive role of BASP1 which was recently also reported for human cancer, small compounds or peptides based on the BASP1 effector domain could be used in drug development strategies aimed at tumors with high MYC expression.

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Section: Introductionmentioning

confidence: 99%

The brain acid‐soluble protein 1 (BASP1) interferes with the oncogenic capacity of MYC and its binding to calmodulin

et al. 2020

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“…Increasing reports demonstrated that the aberrant expression of lncRNAs exert tumor-promoting or tumor-suppressive effects on different types of cancers [ 8 , 9 ]. Moreover, recent evidence revealed that lncRNAs can be involved in the regulation of several cellular processes, such as cell proliferation, cell cycle, differentiation and apoptosis [ 10 , 11 ]. For example, long noncoding RNA LINC00261 suppresses cell proliferation and invasion and promotes cell apoptosis in human choriocarcinoma [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

The long non-coding RNA LINC00473 contributes to cell proliferation via JAK-STAT3 signaling pathway by regulating miR-195-5p/SEPT2 axis in prostate cancer

Xing

Liu

et al. 2020

Bioscience Reports

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Prostate cancer is a kind of male malignant tumor, which has brought tremendous health threat to men. Prostate cancer is difficult to be cured because of high incidence and metastasis rate. Thereby, it is of great urgency to elucidate the underlying molecular mechanism of prostate cancer for the treatment of this cancer. LINC00473 dysregulation has been observed in many cancers. However, the role of LINC00473 was unknown in prostate cancer. In the current study, we discovered that prostate cancer cells presented high expression of LINC00473, and LINC00473 inhibition limited cell proliferation and the expression of proteins in JAK/STAT3 signaling pathway. Additionally, LINC00473 acted as an up-stream factor for miR-195-5p to negatively modulate miR-195-5p expression. Moreover, SEPT2 interacted with miR-195-5p in prostate cancer and SEPT2 expression was positively modulated by LINC00473 and negatively regulated by miR-195-5p. Last, the inhibitory effect of LINC00473 knockdown on cell proliferation and expression of proteins of JAK-STAT3 signaling pathway was restored by SEPT2 overexpression. All in all, LINC00473 contributed to cell proliferation via JAK-STAT3 signaling pathway by regulating miR-195-5p/SEPT2 axis in prostate cancer, which provided a novel therapeutic tactic for prostate cancer patients.

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“…Increasing evidence indicates that lncRNAs are crucial factors in tissue physiology and the pathological processes of various diseases, including cancer (6,7). A large number of dysregulated lncRNAs have been identified in cancer, suggesting their oncogenic or tumor-suppressive properties (8,9). lncRNAs have been reported to serve an important role in the oncogenesis and progression of TC (10,11).…”

Section: Introductionmentioning

confidence: 99%

Long non‑coding RNA H19 knockdown inhibits the cell viability and promotes apoptosis of thyroid cancer cells through regulating the PI3K/AKT pathway

Jin

et al. 2019

Exp Ther Med

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Certain long non-coding (lnc)RNAs have been reported to serve important roles in the genesis and progression of thyroid cancer (TC). Recent studies have demonstrated that the expression of lncRNA H19 is upregulated in TC tissues; however, knowledge of the associated molecular mechanisms is limited. Therefore, the present study aimed to clarify the roles of H19 in TC. The mRNA expression of lncRNA H19 in TC tissues was determined using reverse transcription-quantitative polymerase chain reaction analysis, and the effects of H19 knockdown on cell viability and apoptosis in vitro were assessed using MTT and flow cytometric assays, respectively. Finally, the signaling pathways involved in the effects of H19 were examined. The results indicated that H19 was upregulated in TC tissues. Silencing of H19 inhibited the cell viability and promoted apoptosis of FTC-133 and TPC-1 TC cells, accompanied by an increased expression of B-cell lymphoma 2 (Bcl-2)-associated X protein and caspase 3, and repressed expression of Bcl-2. The results of western blot analysis suggested that the levels of phosphorylated phosphoinositide-3 kinase (PI3K) and phosphorylated AKT were attenuated by H19 silencing. These results suggest that lncRNA H19 exerts an oncogenic function in TC, in part through the PI3K/AKT pathway.

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A new long noncoding RNA (lncRNA) is induced in cutaneous squamous cell carcinoma and down-regulates several anticancer and cell differentiation genes in mouse

Cited by 30 publications

References 62 publications

The brain acid‐soluble protein 1 (BASP1) interferes with the oncogenic capacity of MYC and its binding to calmodulin

The brain acid‐soluble protein 1 (BASP1) interferes with the oncogenic capacity of MYC and its binding to calmodulin

The long non-coding RNA LINC00473 contributes to cell proliferation via JAK-STAT3 signaling pathway by regulating miR-195-5p/SEPT2 axis in prostate cancer

Long non‑coding RNA H19 knockdown inhibits the cell viability and promotes apoptosis of thyroid cancer cells through regulating the PI3K/AKT pathway

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