Bin Zhao

Mesenchymal stem cells (MSCs)-based therapies are promising therapeutic strategies for cancer treatment, because of their strong immunomodulatory and tissue regeneration abilities. In case of colorectal cancer (CRC), MSCs indicate a double-edged sword activity. Some reports declared the inhibitory effects of MSCs on the proliferation, migration, and infiltration of cancer cells to suppress the CRC initiation and development, whereas others showed the tumor-promoter impacts of MSCs on the progression of CRC. Recent investigations have revealed that exosomal microRNAs (Exo-miRs) derived from MSCs (MSCs-Exo-miRs) are attributed to such paradoxical effect. Thus, the current review aimed to seek the role of MSCs-Exo-miRs in CRC progression and their therapeutic potential for the CRC treatment. Cite this article as: Yao H, Sun C, Wang C, et al. The double-edged sword property of mesenchymal stem cell-derived exosomal microRNAs in colorectal cancer. Turk J Gastroenterol. 2024;35(10):755-762.

Purpose: Ubiquitin‐specific peptidase 10 (USP10) has been found to have oncogenic activity in several human tumors. This study first revealed the exact function of USP10 on the progression of thyroid cancer (THCA) by researching its effect on the ferroptosis. Methods: USP10 expression in THCA patients was analyzed by online data analysis and in 75 THCA cases was scrutinized by real‐time quantitative reverse transcription‐polymerase chain reaction and Western blot. Influence of USP10 on the viability, colony formation, migration and invasion of THCA cells was demonstrated by cell counting kit‐8, colony formation, wound healing and Transwell invasion assays. Effect of USP10 on the Erastin‐induced ferroptosis in THCA cells was evaluated by detecting the ferroptosis‐related indicators. Intrinsic mechanism of USP10, glutathione peroxidase 4 (GPX4) and sirtuin 6 (SIRT6) in regulating THCA progression was identified. In vivo xenograft experiment was implemented. Results: USP10 was abundantly expressed in THCA patients, linking to poor outcome. USP10 overexpression enhanced the viability, colony formation, migration and invasion of THCA cells. USP10 mitigated the Erastin‐induced ferroptosis in THCA cells, decreased the levels of iron, Fe ²⁺ , malondialdehyde, lipid reactive oxygen species, reduced mitochondrial superoxide level, and increased mitochondrial membrane potential. USP10 facilitated the expression of ferroptosis suppressor GPX4 by elevating SIRT6. Loss of USP10 repressed the in vivo growth of THCA cells. Conclusion: USP10 might attenuate the ferroptosis to promote thyroid cancer malignancy by facilitating GPX4 via elevating SIRT6. It might be novel target for the treatment of THCA.

Background: Tripartite motif‐containing 29 (TRIM29) has been found to be involved in the regulation of cancer progression and its function varies depending on the type of cancer. However, the role of TRIM29 in cholangiocarcinoma has yet to be revealed. Purpose: This study initially explored the role of TRIM29 in cholangiocarcinoma. Methods: TRIM29 expression in cholangiocarcinoma cells were scrutinized by quantitative real‐time reverse transcription polymerase chain reaction and Western blot. The function of TRIM29 on cholangiocarcinoma cell viability, proliferation, migration and sphere formation abilities were studied by cell count kit‐8, clone formation, Transwell and sphere formation assays. TRIM29 effect on the expression of proteins associated with epithelial‐mesenchymal transition and cancer stem cell characteristics were researched by Western blot. TRIM29 effect on MAPK and β‐catenin pathway activity was researched through Western blot. Results: TRIM29 was overexpressed in cholangiocarcinoma cells. TRIM29 silencing mitigated the viability, proliferation, migration and sphere formation abilities of cholangiocarcinoma cells, increased E‐cadherin expression and decreased the expression of N‐cadherin, Vimentin, CD33, Sox2 and Nanog proteins in cholangiocarcinoma cells. The loss of TRIM29 suppressed the expression of p‐MEK1/2/MEK1/2 and p‐ERK1/2/ERK1/2 in cholangiocarcinoma cells. The inhibition of the MAPK and β‐catenin signaling pathways abrogated the promotion of TRIM29 on cholangiocarcinoma cell viability, proliferation, migration, EMT, and cancer stem cell characteristics. Conclusion: TRIM29 plays an oncogenic role in cholangiocarcinoma. It may promote the malignancy of cholangiocarcinoma via inducing the activation of the MAPK and β‐catenin pathways. Thus, TRIM29 may aid in the creation of innovative treatment strategies for cholangiocarcinoma.

This study researched the exact function of IgG1 heavy chain (IGHG1) on breast cancer (BC) progression. IGHG1 level within BC and paired normal tissues was acquired in Gene Expression Profiling Interactive Analysis dataset. Meanwhile, this work harvested tumor and paired healthy tissues in 42 BC cases. siRNA targeting IGHG1 was transfected into BC cells. SC79 was used to treat the transfected BC cells. CCK-8 assay, clone formation experiment, BrdU assay, Transwell experiment and flow cytometry were carried out to measure the viability, colony formation, proliferation, invasion, and apoptosis of BC cells. Paclitaxel and cisplatin sensitivity of BC cells was evaluated by MTT assay. Real-time quantitative reverse transcription-polymerase chain reaction and Western-blot were performed for measuring mRNA and protein expression. The overexpressed IGHG1 indicated dismal BC survival. IGHG1 silencing attenuated the viability, invasion, proliferation, epithelial-mesenchymal transition, but enhanced the apoptosis of BC cells. IGHG1 silencing enhanced the paclitaxel and cisplatin sensitivity of BC cells. IGHG1 silencing suppressed the activity of the MEK, AKT, and ERK pathways. AKT agonist partially reversed the inhibition of IGHG1 silencing on BC cell malignant phenotype and resistance to paclitaxel and cisplatin. IGHG1 promotes the malignant development of BC by activating the AKT pathway. It may be an effective target for BC treatment.

This study aimed to explore the role and potential mechanism of the long non-coding (lncRNA) MBNL1-AS1 in human breast cancer. We included 80 patients with breast cancer in this study. Breast cancer cell lines, including MCF7, SKBR3, MDA-MB-231 and MDA-MB-415, and the normal human breast cell line MCF10A were used in this study. MBNL1-AS1, miR-889-3p mimics, si-Krüppel-like factor 9 (KLF9) or their controls were transfected in the cells. Quantitative reverse transcription polymerase chain reaction (qRT-PCR), Western blotting and immunohistochemistry assay were performed to detect the expression of MBNL1-AS1, miR-889-3p and KLF9. Cell proliferation, invasion and migration were detected. Luciferase reporter gene and pull-down assay were performed to verify the target relationship among MBNL1-AS1, miR-889-3p and KLF9. Glycolysis was also detected after transfection. The expression of the lncRNA MBNL1-AS1 was low in the breast cancer tissues and cells. Lower expression levels of the lncRNA MBNL1-AS1 were associated with poor prognosis of breast cancer. Overexpression of the lncRNA MBNL1-AS1 decreased proliferation, invasion, migration and glycolysis of breast cancer cells. The lncRNA MBNL1-AS1 could interact with miR-889-3p, and KLF9 was the downstream target of miR-889-3p. Moreover, miR-889-3p was negatively correlated with KLF9 and lncRNA MBNL1-AS1. Both miR-889-3p and si-KLF9 could reverse the overexpression of lncRNA MBNL1-AS1 in breast cancer development. The lncRNA MBNL1-AS1 decreased proliferation, invasion, migration and glycolysis of breast cancer via the miR-889-3p/KLF9 axis, which might be a potential biomarker for the diagnosis of breast cancer.

Su Z, et al. Yonsei Med J. 2022 Jun;63(6):591-600. https://doi.org/10.3349/ymj.2022.63.6.591

Introduction: Acne is one of the commonest skin disorders. During Adolescence 70% to 80% of the population have some clinically evident acne [1]. This is commonly seen as oily face, obstructive horny plugs or inflammatory lesions like pustules. These may complicate into cysts, abscesses, scars, keloids, hyper-pigmentation and above all psychological damage to self-confidence. The striking feature of acne is greasy skin and severity of acne is directly proportional to sebum excretion rate SER [2].

Long non‑coding RNA (lncRNA) FLVCR1 antisense RNA 1 (FLVCR1‑AS1) serves a crucial role in many types of cancer; however, to the best of our knowledge, the biological effect of FLVCR1‑AS1 in cholangiocarcinoma (CCA) remains unclear. The present study aimed to elucidate the involvement of FLVCR1‑AS1 in the regulation of human CCA cell growth, migration and invasion, as well as the mechanisms underlying its effect. The expression levels of FLVCR1‑AS1 in CCA tumor tissues, adjacent normal tissues, CCA cell lines and a cholangiocyte cell line were determined by reverse transcription‑quantitative polymerase chain reaction. A significantly higher expression level of FLVCR1‑AS1 was identified in CCA tumor tissues and the CCA cell lines HuCCT1 and CCLP1 compared with the normal controls. Short hairpin RNA targeting FLVCR1‑AS1 (shFLVCR1‑AS1) and a control plasmid (shNC) were transfected into CCA cell lines. Cell proliferation, colony formation, migration and invasion of CCA cells transfected with shFLVCR1‑AS1 were significantly suppressed compared with the shNC groups. The expression levels of migration and invasion‑associated proteins, including Twist, matrix metalloproteinase (MMP)‑2 and MMP‑9, were also significantly suppressed by shFLVCR1‑AS1‑treatment. Furthermore, FLVCR1‑AS1 knockdown inhibited tumor growth in a xenograft model. Mechanistically, FLVCR1‑AS1 was demonstrated to sponge microRNA‑485‑5p (miR‑485‑5p) in human CCA. The expression of miR‑458‑5p was significantly decreased in CCA tissue compared with normal tissue, and Pearson's correlation analysis revealed that FLVCR1‑AS1 expression was negatively correlated with miR‑485‑5p expression in CCA tissues. These results suggested that lncRNA FLVCR1‑AS1 may be used as a novel therapeutic target and a potential diagnostic marker for CCA.

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