@article{ author = {Hariyanto, Narendra Ichiputra and Yo, Edward Christopher and Wanandi, Septelia Inawati}, title = {Regulation and Signaling of TGF-β Autoinduction}, abstract ={Cell signaling is a vital part of biological life. It helps coordinating various cellular processes including cell survival, cell growth, cell death, and cell interaction with the microenvironment and other cells. In general, cell signaling involves the attachment of signaling molecules known as ligands to specific receptors on cell surface, which then activate downstream events that dictate the cell’s response. One of the most studied ligands is transforming growth factor-beta (TGF-β). TGF-β signaling is mainly mediated by suppressor of mothers against decapentaplegic (Smad) proteins, but it also interacts with other pathways such as the Ras and mitogen-activated protein kinase (MAPK) signaling pathways. Furthermore, TGF-β can have a dual role depending on the cellular and microenvironmental context, in which it can act as either a growth promoter or a growth inhibitor. It has been known that TGF-β can self-induce its ligand production, thereby prolonging and amplifying its effect on cells and their microenvironment. The aim of this review is to discuss the regulation and signaling of TGF-β autoinduction, which still remain to be elucidated. Several factors have been found to facilitate TGF-β autoinduction, which include the activator protein-1 (AP1) complex, Smad3-dependent signaling, and non-Smad signaling pathways. On the other hand, the LIM (Lin11, Isl-1 and Mec-3) domain only 7 (LMO7) protein can suppress TGF-β autoinduction by interfering with the activities of AP-1 and Smad3. Since TGF-β autoinduction is implicated in various pathological conditions, better understanding of its regulation and signaling can provide new directions for therapy.}, Keywords = {Cell signaling, TGF-β, TGF-β receptors, autoinduction, signaling pathways, Smad-dependent signaling, non-Smad-dependent signaling}, volume = {10}, Number = {4}, pages = {234-247}, publisher = {Babol University of Medical Sciences}, title_fa = {}, abstract_fa ={}, keywords_fa = {}, doi = {10.22088/IJMCM.BUMS.10.4.234}, url = {http://ijmcmed.org/article-1-1787-en.html}, eprint = {http://ijmcmed.org/article-1-1787-en.pdf}, journal = {International Journal of Molecular and Cellular Medicine (IJMCM)}, issn = {2251-9637}, eissn = {2251-9645}, year = {2021} } @article{ author = {Tran, Manh Tie}, title = {Retraction notice: Roles of Renin-Angiotensin System in the Regulation of Prostate Cancer Bone Metastasis: A Critical Review}, abstract ={By this notice, the Editor in chief of the International Journal of Molecular and Cellular Medicine (IJMCM) retracts from publication the following review article: "Roles of renin-angiotensin system in the regulation of prostate cancer bone metastasis: a critical review" authored by Tran Tien Manh due to duplicate submission. The manuscript was submitted to IJMCM on 11 August 2021 and accepted on 7 December 2021. The author was asked on 29 December 2021 through the process of proof finalization whether he performed a duplicate publication to Annals of Urologic Oncology which published a similar article  2021, 4(1): 31-41. https://doi.org/10.32948/auo.2021.10.20 (submitted 31 Aug 2021; accepted 7 Oct 2021; published online: 15 Oct 2021), or any unauthorized publication underwent with that journal. According to authors' explanations, it appeared that he deliberately made a duplicate submission which is unethical and a case of self-plagiarism that causes a waste of editorial and reviewers time and resources, and avoids other authors to publish their manuscript by unfairly taking up limited journal space. The author still claims that this duplicate submission was unintended and an unexpected accident. The Editor in chief apologizes to the readership for this unfortunate incident and any inconvenience caused.}, Keywords = {}, volume = {10}, Number = {4}, pages = {248-248}, publisher = {Babol University of Medical Sciences}, title_fa = {}, abstract_fa ={}, keywords_fa = {}, doi = {10.22088/IJMCM.BUMS.10.4.248}, url = {http://ijmcmed.org/article-1-1730-en.html}, eprint = {http://ijmcmed.org/article-1-1730-en.pdf}, journal = {International Journal of Molecular and Cellular Medicine (IJMCM)}, issn = {2251-9637}, eissn = {2251-9645}, year = {2021} } @article{ author = {Dabiri, Arezou and Sharifi, Mohammadreza and Sarmadi, Akram}, title = {Knockdown of SOX12 Expression Induced Apoptotic Factors is Associated with TWIST1 and CTNNB1 Expression in Human Acute Myeloid Leukemia Cells}, abstract ={Recent improvements in molecular treatment and gene therapy led to discovering novel cancer remedies. Antisense LNA GapmeRs is a state-of-the-art molecular research field for diagnosing and treating various cancer types. Acute myeloid leukemia (AML) is a heterogeneous hematopoietic malignancy defined by the rapid accumulation and malignant proliferation of immature myeloid progenitors. SOX12 is a new potential target for acute myeloid leukemia.  In this study, SOX12 was blocked by antisense LNA GapmeRs (ALG) in human AML cell lines (KG1 and M07e). Cells were transfected with Gapmer anti-SOX12 at 24, 48, and 72 h post-transfection. Transfection efficiency was assessed by a fluorescent microscope. Furthermore, evaluation of SOX12, TWIST1, CTNNB1, CASP3, and CASP9 expression was performed by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). Cell viability was determined by MTT assay. SOX12 expression was decreased remarkably in the ALG group. Moreover, SOX12 knockdown was associated with a decrease in TWIST1 and CTNNB1 expression. Besides, downregulation of SOX12 in both cell lines could induce apoptosis, probably through upregulation of CASP3 and CASP9. The findings reveal that SOX12 knockdown could be a new target for reducing AML cells proliferation through antisense therapy approach.}, Keywords = {Acute myeloblastic leukemia, antisense LNA GapmeRs, SOX12, TWIST1, CTNNB1, apoptosis}, volume = {10}, Number = {4}, pages = {249-257}, publisher = {Babol University of Medical Sciences}, title_fa = {}, abstract_fa ={}, keywords_fa = {}, doi = {10.22088/IJMCM.BUMS.10.4.249}, url = {http://ijmcmed.org/article-1-1770-en.html}, eprint = {http://ijmcmed.org/article-1-1770-en.pdf}, journal = {International Journal of Molecular and Cellular Medicine (IJMCM)}, issn = {2251-9637}, eissn = {2251-9645}, year = {2021} } @article{ author = {AmeliMojard, Melika and AmeliMojarad, Mandana and Pourmahdian, Alirez}, title = {Long Non-coding RNA snaR Promotes Proliferation in EGFR Wild Type Non-Small Cell Lung Cancer Cells}, abstract ={Lung cancer is the second most common cancer and has high morbidity and mortality worldwide with non-small cell lung cancer (NSCLC) accounting for 85% of the cases. Over-expression of epidermal growth factor receptor (EGFR) has been clarified in different cancers, and has been shown to have a crucial role in tumor progression. In this study, we evaluated long non-coding RNA small NF90-associated RNA (snaR) expression in different EGFR-statue cell lines. Knockdown experiments were conducted to analyze snaR expression in selected cell lines. MTT and transwell assays were respectively employed to evaluate the proliferative and invasive abilities of NSCLC cells. The expression of snaR was remarkably up-regulated in SPC-A1 and A549 wild-type EGFR cell lines. Down regulation of snaR with small interfering RNA significantly inhibited cell invasion as well as proliferation of SPC-A1 and A549 cells. Our results indicate that snaR may be a potential therapeutic biomarker for NSCLC.}, Keywords = {Long non-coding RNA, snaR, non-smallcell lung carcinoma, EGFR}, volume = {10}, Number = {4}, pages = {258-264}, publisher = {Babol University of Medical Sciences}, title_fa = {}, abstract_fa ={}, keywords_fa = {}, doi = {10.22088/IJMCM.BUMS.10.4.258}, url = {http://ijmcmed.org/article-1-1670-en.html}, eprint = {http://ijmcmed.org/article-1-1670-en.pdf}, journal = {International Journal of Molecular and Cellular Medicine (IJMCM)}, issn = {2251-9637}, eissn = {2251-9645}, year = {2021} } @article{ author = {GhorbanKhanTafreshi, Mostafa and Mazaheri, Zohreh and Heidari, Mansour and Babaei, Nahid and Doosti, Abbas}, title = {Induction of Apoptosis in the U937 Cell Line Co-cultured with Adipose-derived Stem Cells Secreting Bone Morphogenetic Protein-4}, abstract ={Transforming growth factor-beta (TGF-β) plays a significant role in tumorigenesis. MiR-181b is a multifunctional miRNA involved in numerous cellular processes, such as cell fate and cell invasion. This study aimed to examine whether the co-culture of adipose-derived stem cells (ADSCs), highly expressing bone morphogenetic protein-4, with the U937 cell line, which is a human myeloid leukemia cell line, is able to induce cell death in this cancer cell line, considering the potential ability of ADSCs to migrate from tumor sites. Cell surface markers, namely CD73 and CD105, were analyzed to verify the identity of mesenchymal stem cells isolated from adipose tissue. Besides, the osteogenic and adipogenic differentiation potentials of ADSCs were evaluated. The induction of cell death and apoptosis in the U937 cell line was assessed using MTT and annexin V/ PI assays, respectively. The expression levels of miR-181 and TGF-b were determined in the co-culture system using real-time PCR. The results of MTT and annexin V/ PI assays showed that BMP4-expressing ADSCs could inhibit cell viability and induce apoptosis in U937 cells in the co-culture system. The co-culture of ADSCs, highly expressing BMP-4, with the U937 cell line led to the downregulation of miR-181 and TGF-β genes in the human cancer cell line. ADSCs may further be studied as a candidate for the treatment of hematological cancers.  }, Keywords = {Stem cells, cancer, miR-181, TGF-β, apoptosis}, volume = {10}, Number = {4}, pages = {265-276}, publisher = {Babol University of Medical Sciences}, title_fa = {}, abstract_fa ={}, keywords_fa = {}, doi = {10.22088/IJMCM.BUMS.10.4.265}, url = {http://ijmcmed.org/article-1-1758-en.html}, eprint = {http://ijmcmed.org/article-1-1758-en.pdf}, journal = {International Journal of Molecular and Cellular Medicine (IJMCM)}, issn = {2251-9637}, eissn = {2251-9645}, year = {2021} } @article{ author = {Fogen, Dawso}, title = {The Role of PaFicT in Pseudomonas aeruginosa Persister Cell Formation}, abstract ={The opportunistic pathogen Pseudomonas aeruginosa (Pa) is a major concern for immunocompromised and cystic fibrosis patients. Chronic lung infections caused by Pa are generally considered incurable, in part, due to the bacteria’s ability to form persister cells. These variants are categorized as being phenotypically dormant and highly tolerant to antibiotic treatment. Currently, the mechanisms involved in Pa persister cell formation is poorly understood. One promising candidate is the Pa filamentation induced by cAMP (FIC) domain containing toxin (PaFicT), which like other FIC toxins transiently inhibits cell growth. Genetic knockout and complementation by single copy chromosomal insertion was used to characterize paficT involvement in Pa persister cell formation. Toxicity and the PaFicT active site were examined by overexpression of wild-type and mutant protein variants. Antibiotic tolerance of PaFicT-induced Pa persister cells, was measured by minimum inhibitory concentration (MIC) analysis and compared to parental mostly non-persister populations. Deletion of paficT resulted in a 7.2-fold reduction in persister cell formation, which was fully complemented by re-insertion of the gene. Expression of PaFicT significantly increased persister cell formation by 5.9-fold, and this phenotype required a functional FIC active site motif. Unlike growing cell populations, PaFicT-induced persister cells were unaffected by 4 h treatment with 10 × MIC meropenem and showed an increased survival of 6.2 × 105-fold to tobramycin under the same conditions. Alternatively, survival of both persisters and parental, mostly non-persister, populations were below detectable levels following amikacin treatment. Results indicate a potential major involvement of PaFicT in Pa persister cell formation and multidrug tolerance.  }, Keywords = {Drug resistance, Pseudomonas, cystic fibrosis}, volume = {10}, Number = {4}, pages = {277-287}, publisher = {Babol University of Medical Sciences}, title_fa = {}, abstract_fa ={}, keywords_fa = {}, doi = {10.22088/IJMCM.BUMS.10.4.277}, url = {http://ijmcmed.org/article-1-1783-en.html}, eprint = {http://ijmcmed.org/article-1-1783-en.pdf}, journal = {International Journal of Molecular and Cellular Medicine (IJMCM)}, issn = {2251-9637}, eissn = {2251-9645}, year = {2021} } @article{ author = {Heidari, Soran and Azizbeigi, Kamal and Bahmanpour, Kaveh}, title = {MicroRNA-145, Wnt3a, and Dab2 Genes Expression Changes of the Cardiomyocytes in Hypercholesterolemic Rats Exposed to the Aerobic Training}, abstract ={The current study aimed to investigate the effect of a 12-week endurance training (ET) on microRNA-145 (miR-145) changes and Wnt3a and Dab2 cardiomyocytes genes expression of hypercholesterolemic Wistar male rats. Thirty-two male Wistar rats (191.2±19 g, 6-8 weeks age) were randomly assigned into the aerobic exercise-normal nutrition (ANN; n=8), hypercholesterolemic (HCL; n=8), aerobic exercise- hypercholesterolemic (ACL; n=8), and normal nutrition (NN; n=8). Hypercholesterolemia was created by adding 1% cholesterol to the food of the HCL and ACL rats. ET was done five sessions per week on nonconsecutive days for 12 weeks. Twenty-four hours after the last training session, the rats were killed, and the cardiomyocytes were removed.  The expression of miR-145, Wnt3a, and Dab2 genes in cardiomyocytes was assessed by real time PCR method. The expression of miR-145 significantly increased in the ANN group in comparison with other groups (P = 0.001). Also, Dab2 gene expression significantly decreased in the ANN group in comparison with ACL (P = 0.001) and HCL (P = 0.001) groups. The results also showed that the Wnt3a in the ANN group was significantly different from NN (p=0.001), ACL, and HCL (p=0.001) groups. It can be concluded that aerobic training and cholesterol-rich foods play an essential regulatory role in the expression of miR-145, Dab2, and Wnt3a genes. However, cholesterol-rich foods appear to play a more significant regulatory role than aerobic exercise training.     }, Keywords = {Diet, high-fat, myocytes, cardiac, miR145, microRNA}, volume = {10}, Number = {4}, pages = {288-296}, publisher = {Babol University of Medical Sciences}, title_fa = {}, abstract_fa ={}, keywords_fa = {}, doi = {10.22088/IJMCM.BUMS.10.4.288}, url = {http://ijmcmed.org/article-1-1545-en.html}, eprint = {http://ijmcmed.org/article-1-1545-en.pdf}, journal = {International Journal of Molecular and Cellular Medicine (IJMCM)}, issn = {2251-9637}, eissn = {2251-9645}, year = {2021} }