es/iode’s Post

📃Scientific paper: Suppression of the long non-coding RNA LINC01279 triggers autophagy and apoptosis in lung cancer by regulating FAK and SIN3A Abstract: Long non-coding RNAs play critical roles in the development of lung cancer by functioning as tumor suppressors or oncogenes. Changes in the expression of LINC01279 have been associated with cell differentiation and human diseases. However, the mechanism underlying LINC01279 activity in tumorigenesis is not clear. Here, we analyzed the function of LINC01279 in lung adenocarcinoma using clinical samples, xenografts, and non-small-cell lung cancer cell lines. We found that LINC01279 is highly expressed in lung adenocarcinoma and may be considered as a predictive factor for this cancer. Knockdown of LINC01279 prevents tumor growth in xenografts and in cancer cell lines by activating autophagy and apoptosis. Molecularly, we revealed that LINC01279 regulates the expression of focal adhesion kinase and extracellular-regulated kinase signaling. In addition, it complexes with and stabilizes the transcriptional co-repressor SIN3A protein. Suppression of focal adhesion kinase and SIN3A also induces apoptosis and prevents tumor progression, suggesting that they may at least in part mediate the oncogenic activity of LINC01279 . These results identify LINC01279 as a possible oncogene that plays an important role in the development of lung cancer. Our findings provide insights into the mechanism underlying LINC01279 -mediated oncogenesis of lung adenocarcinoma. They may help to discover potential therapeutic targets for cancer diagnosis and prognosis. Continued on ES/IODE ➡️ https://etcse.fr/Qbo ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.

📃Scientific paper: Circular RNA hsa_circ_0000144 aggravates ovarian Cancer progression by regulating ELK3 via sponging miR-610 Abstract: Background Ovarian cancer is a common cause of death among women and a health problem worldwide. Circ_0000144 has been confirmed to be an oncogene involved in cancer progression, such as gastric cancer. However, the role of circ_0000144 in ovarian cancer remains unclear and needs to be elucidated. This retrospective study aimed to investigate the underlying mechanism of circ_0000144 in ovarian cancer. Methods Differentially expressed circ_0000144 expression in ovarian cancer and normal tissues was identified by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). In vitro assays were performed to explore the biological functions of circ_0000144 in ovarian cancer cells. An in vivo xenograft model was used to investigate the efficacy of circ_0000144 in the progression of ovarian cancer. Results Circ_0000144 was significantly upregulated in ovarian cancer cells and tissues. Circ_0000144 overexpression significantly promoted ovarian cancer cell proliferation, migration, and invasion. This study further demonstrated that circ_0000144 downregulated ELK3 levels by sponging miR-610 in ovarian cancer cells. Moreover, circ_0000144 significantly promotes ovarian cancer tumorigenesis in vivo. Conclusion Our data indicate that circ_0000144 could enhance the carcinogenesis of ovarian cancer by specifically targeting miR-610, which may serve as a novel target for the diagnosis and prognosis of ovarian cancer. Continued on ES/IODE ➡️ https://etcse.fr/ECTV ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.

📃Scientific paper: A zebrafish xenotransplant model of anaplastic thyroid cancer to study the tumor microenvironment and innate immune cell interactions in vivo Abstract: Anaplastic thyroid cancer (ATC) is a rare malignant subtype of thyroid cancer. While ATC is rare it accounts for a disproportionately high number of thyroid cancer-related deaths. Here we developed an ATC xenotransplant model in zebrafish larvae, where we can study tumorigenesis and therapeutic response in vivo. Using both mouse (T4888M) and human (C643) derived fluorescently labeled ATC cell lines we show these cell lines display different engraftment rates, mass volume, proliferation, and angiogenic potential. Next, using a PIP-FUCCI reporter to track proliferation in-vivo we observed cells in each phase of the cell cycle. Additionally, we performed long-term non-invasive intravital microscopy over 48 hours to understand cellular dynamics in the tumor microenvironment at the single cell level. Lastly, we tested a well-known mTOR inhibitor to show our model could be used as an effective screening platform for new therapeutic compounds. Altogether, we show that zebrafish xenotransplants make a great model to study thyroid carcinogenesis and the tumor microenvironment, while also being a suitable model to test new therapeutics in vivo . SUMMARY STATEMENT: Anaplastic thyroid cancer xenotransplant model in zebrafish larvae to study thyroid cancer tumorigenesis and tumor microenvironment. Using confocal microscopy to understand cell cycle progression, interactions with the innate immune system, and test therapeutic compounds in vivo. Continued on ES/IODE ➡️ https://etcse.fr/SL0W ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.

📃Scientific paper: A zebrafish xenotransplant model of anaplastic thyroid cancer to study the tumor microenvironment and innate immune cell interactions in vivo Abstract: Anaplastic thyroid cancer (ATC) is a rare malignant subtype of thyroid cancer. While ATC is rare it accounts for a disproportionately high number of thyroid cancer-related deaths. Here we developed an ATC xenotransplant model in zebrafish larvae, where we can study tumorigenesis and therapeutic response in vivo. Using both mouse (T4888M) and human (C643) derived fluorescently labeled ATC cell lines we show these cell lines display different engraftment rates, mass volume, proliferation, and angiogenic potential. Next, using a PIP-FUCCI reporter to track proliferation in-vivo we observed cells in each phase of the cell cycle. Additionally, we performed long-term non-invasive intravital microscopy over 48 hours to understand cellular dynamics in the tumor microenvironment at the single cell level. Lastly, we tested a well-known mTOR inhibitor to show our model could be used as an effective screening platform for new therapeutic compounds. Altogether, we show that zebrafish xenotransplants make a great model to study thyroid carcinogenesis and the tumor microenvironment, while also being a suitable model to test new therapeutics in vivo . SUMMARY STATEMENT: Anaplastic thyroid cancer xenotransplant model in zebrafish larvae to study thyroid cancer tumorigenesis and tumor microenvironment. Using confocal microscopy to understand cell cycle progression, interactions with the innate immune system, and test therapeutic compounds in vivo. Continued on ES/IODE ➡️ https://etcse.fr/SL0W ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.

📃Scientific paper: Elevated LINC00894 relieves the oncogenic properties of thyroid cancer cell by sponging let-7e-5p to promote TIA-1 expression Abstract: LINC00894 plays an important role in cancer cell proliferation and invasion in breast and kidney cancer. However, its role in thyroid cancer proliferation and metastasis remains unclear. In this study, data on LINC00894 expression in thyroid cancer tissues were obtained from GEPIA2. miRNA expression in thyroid cancer tissues was obtained from starBase 3.0 and OncomiR. Cell proliferation was evaluated using CCK-8, and Transwell chambers were used for the migration and invasion assays. LINC00894 and let-7e-5p expressions in thyroid cancer cells were measured using qRT–PCR. Meanwhile, TIA-1 expression in thyroid cancer cells was analyzed via western blotting. We found that LINC00894 expression was markedly reduced in thyroid cancer tissues and cells, and low expression of LINC00894 was associated with poor prognosis in thyroid cancer. LINC00894 overexpression inhibited the proliferation, migration, and invasion of CAL-62 and TPC-1 cells. Additionally, let-7e-5p expression was substantially enhanced in CAL-62 and TPC-1 cells. LINC00894 overexpression promoted TIA-1 expression by acting as a sponge of let-7e-5p. Finally, let-7e-5p weakened the function of LINC00894 in thyroid cancer cells via reduction in TIA-1 levels. In conclusion, our data suggest that increased LINC00894 expression reduces the oncogenic properties of thyroid cancer cells by sponging let-7e-5p to promote TIA-1 expression. Continued on ES/IODE ➡️ https://etcse.fr/c4ht ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.

📃Scientific paper: BCKDK regulates breast cancer cell adhesion and tumor metastasis by inhibiting TRIM21 ubiquitinate talin1 Abstract: Breast cancer is the most common malignant cancer in women worldwide. Cancer metastasis is the major cause of cancer-related deaths. BCKDK is associated with various diseases, including proliferation, migration, and invasion in multiple types of human cancers. However, the relevance of BCKDK to the development and progression of breast cancers and its function is unclear. This study found that BCKDK was overexpressed in breast cancer, associated with poor prognosis, and implicated in tumor metastasis. The downregulation of BCKDK expression inhibited the migration of human breast cancer cells in vitro and diminished lung metastasis in vivo. BCKDK perturbed the cadherin-catenin complex at the adherens junctions (AJs) and assembled focal adhesions (FAs) onto the extracellular matrix, thereby promoting the directed migration of breast cancer cells. We observed that BCKDK acted as a conserved regulator of the ubiquitination of cytoskeletal protein talin1 and the activation of the FAK/MAPK pathway. Further studies revealed that BCKDK inhibited the binding of talin1 to E3 ubiquitin ligase-TRIM21, leading to the decreased ubiquitination/degradation of talin1. In conclusion, identifying BCKDK as a biomarker for breast cancer metastasis facilitated further research on diagnostic biomarkers. Elucidating the mechanism by which BCKDK exerted its biological effect could provide a new theoretical basis for developing new markers for breast cancer metastasis and contribute to dev... Continued on ES/IODE ➡️ https://etcse.fr/4nS ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.

📃Scientific paper: CircNDST1 promotes papillary thyroid cancer progression via its interaction with CSNK2A1 to activate the PI3K–Akt pathway and epithelial–mesenchymal transition Abstract: Background Multiple studies have established a strong relationship between circRNA and cancer progression. Cervical lymph node metastasis is a key factor influencing the surgical approach and distant metastasis of papillary thyroid cancer (PTC). However, the role of circNDST1 in PTC has not been investigated. Our research focused on revealing the function and mechanism of action of circNDST1 in PTC. Methods High-throughput sequencing and qPCR were used to assess the expression of circRNA in PTC tissues with extensive cervical lymph node metastasis and circNDST1 in cell lines, respectively. The proliferative effects of circNDST1 in vitro and in vivo were analyzed using CCK8, clone formation assay, EdU, and nude mouse tumorigenesis assay. The transwell scratch assay was employed in the scrutiny of the effect of circNDST1 on the migration and invasion abilities of thyroid cancer cells, while circNDST1’s influence on the PI3K–Akt pathway and the Epithelial–Mesenchymal Transition (EMT) key protein expression was evaluated utilizing RNA sequencing and western blot. RNA pull-down and RIP were used to examine the binding of circNDST1 to CSNK2A1. Results CircNDST1 was highly expressed in PTC cell lines, but knocking it down inhibited the proliferation, migration, and invasive abilities of TPC1 and KTC1 cell lines. CircNDST1 bonded with CSNK2A1 and promoted the interaction between CSNK2A1 and Akt, leading to the activation of the PI3K–Akt pathway and EMT. Conclusion CircNDS... Continued on ES/IODE ➡️ https://etcse.fr/viP ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.

A key finding: Silencing of SIRPα enhances the antitumor efficacy of CAR-M in solid tumor. This should be evaluated in clinical setting. The potential of macrophage-mediated phagocytosis as a cancer treatment is promising. Blocking the CD47–SIRPα interaction with a CD47-specific antibody significantly enhances macrophage phagocytosis. However, concerns regarding their toxicity to nontumor cells remain substantial. Here, we engineered chimeric antigen receptor macrophages (CAR-Ms) by fusing a humanized single-chain variable fragment with FcγRIIa and integrating short hairpin RNA to silence SIRPα, thereby disrupting the CD47–SIRPα signaling pathway. These modified CAR-shSIRPα-M cells exhibited an M1-like phenotype, superior phagocytic function, substantial cytotoxic effects on HER2-positive tumor cells, and the ability to eliminate patient-derived organoids. In vivo, CAR-M cells significantly inhibited tumor growth and prolonged survival in tumor-bearing mice. Notably, CAR-shSIRPα-M cells enhanced cytotoxic T-cell infiltration into tumors, thereby enhancing the antitumor response in both the humanized immune system mouse model and immunocompetent mice. Mechanistically, SIRPα inhibition activated inflammatory pathways and the cGAS-STING signaling cascade in CAR-M cells, leading to increased production of proinflammatory cytokines, reactive oxygen species, and nitric oxide, thereby enhancing their antitumor effects. These findings underscore the potential of SIRPα inhibition as a novel strategy to increase the antitumor efficacy of CAR-M cells in cancer immunotherapy, particularly against solid tumors. https://lnkd.in/ekzMKtzS

📃Scientific paper: CircNDST1 promotes papillary thyroid cancer progression via its interaction with CSNK2A1 to activate the PI3K–Akt pathway and epithelial–mesenchymal transition Abstract: Background Multiple studies have established a strong relationship between circRNA and cancer progression. Cervical lymph node metastasis is a key factor influencing the surgical approach and distant metastasis of papillary thyroid cancer (PTC). However, the role of circNDST1 in PTC has not been investigated. Our research focused on revealing the function and mechanism of action of circNDST1 in PTC. Methods High-throughput sequencing and qPCR were used to assess the expression of circRNA in PTC tissues with extensive cervical lymph node metastasis and circNDST1 in cell lines, respectively. The proliferative effects of circNDST1 in vitro and in vivo were analyzed using CCK8, clone formation assay, EdU, and nude mouse tumorigenesis assay. The transwell scratch assay was employed in the scrutiny of the effect of circNDST1 on the migration and invasion abilities of thyroid cancer cells, while circNDST1’s influence on the PI3K–Akt pathway and the Epithelial–Mesenchymal Transition (EMT) key protein expression was evaluated utilizing RNA sequencing and western blot. RNA pull-down and RIP were used to examine the binding of circNDST1 to CSNK2A1. Results CircNDST1 was highly expressed in PTC cell lines, but knocking it down inhibited the proliferation, migration, and invasive abilities of TPC1 and KTC1 cell lines. CircNDST1 bonded with CSNK2A1 and promoted the interaction between CSNK2A1 and Akt, leading to the activation of the PI3K–Akt pathway and EMT. Conclusion CircNDS... Continued on ES/IODE ➡️ https://etcse.fr/viP ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.

📃Scientific paper: A zebrafish xenotransplant model of anaplastic thyroid cancer to study the tumor microenvironment and innate immune cell interactions in vivo Abstract: Anaplastic thyroid cancer (ATC) is a rare malignant subtype of thyroid cancer. While ATC is rare it accounts for a disproportionately high number of thyroid cancer-related deaths. Here we developed an ATC xenotransplant model in zebrafish larvae, where we can study tumorigenesis and therapeutic response in vivo. Using both mouse (T4888M) and human (C643) derived fluorescently labeled ATC cell lines we show these cell lines display different engraftment rates, mass volume, proliferation, and angiogenic potential. Next, using a PIP-FUCCI reporter to track proliferation in-vivo we observed cells in each phase of the cell cycle. Additionally, we performed long-term non-invasive intravital microscopy over 48 hours to understand cellular dynamics in the tumor microenvironment at the single cell level. Lastly, we tested a well-known mTOR inhibitor to show our model could be used as an effective screening platform for new therapeutic compounds. Altogether, we show that zebrafish xenotransplants make a great model to study thyroid carcinogenesis and the tumor microenvironment, while also being a suitable model to test new therapeutics in vivo . SUMMARY STATEMENT: Anaplastic thyroid cancer xenotransplant model in zebrafish larvae to study thyroid cancer tumorigenesis and tumor microenvironment. Using confocal microscopy to understand cell cycle progression, interactions with the innate immune system, and test therapeutic compounds in vivo. Continued on ES/IODE ➡️ https://etcse.fr/SL0W ------- If you find this interesting, feel free to follow, comment and share. We need your help to enhance our visibility, so that our platform continues to serve you.