OBJECTIVE: Radioresistance is a common problem in the treatment of many cancers, including hepatocellular carcinoma (HCC). Previous studies have shown that circROBO1 is highly expressed in HCC tissues and acts as a cancer promoter to accelerate the malignant progression of HCC. However, the role and mechanism of circROBO1 in HCC radioresistance remain unclear.
METHODS: CircROBO1, microRNA (miR)-136-5p and RAD21 expression levels were analyzed by quantitative real-time PCR. Cell function and radioresistance were evaluated by colony formation assay, cell counting kit 8 assay, EdU assay and flow cytometry. Protein expression was determined using western blot analysis. RNA interaction was analyzed by dual-luciferase reporter assay and RNA pull-down assay. In vivo experiments were performed by constructing mice xenograft models.
RESULTS: CircROBO1 was highly expressed in HCC, and its knockdown inhibited HCC cell proliferation and promoted apoptosis to enhance cell radiosensitivity. On the mechanism, circROBO1 could serve as miR-136-5p sponge to positively regulate RAD21. MiR-136-5p inhibitor or RAD21 overexpression reversed the regulation of circROBO1 knockdown on the radiosensitivity of HCC cells. Also, circROBO1 interference improved the radiosensitivity of HCC tumors in vivo.
CONCLUSIONS: CircROBO1 might be a promising target for treating HCC radioresistance.

Background: Long noncoding RNAs (lncRNAs) contribute to the initiation and progression of gastric cancer (GC). The purpose of this study is to examine the potential role of lncRNA colorectal neoplasia differentially expressed (CRNDE) in modulating the expression of migration and invasion enhancer 1 (MIEN1) through the suppression of miR-136-5p in GC. Methods: The biological roles of CRNDE, miR-136-5p, and MIEN1 in GC were assessed both in laboratory settings and through the examination of clinical samples. Results: CRNDE was found to be significantly increased in GC tissues, and this upregulation was associated with an unfavorable prognosis of GC patients. In vitro experiments showed that inhibiting cell growth and migration, along with promoting apoptosis in GC cells, could be achieved by either disabling CRNDE or MIEN1, or by increasing the expression of miR-136-5p. MIEN1 is a specific recipient of miR-136-5p, and the anticancer effects of miR-136-5p can be counteracted by the increased expression of MIEN1. Through the examination of clinical specimens, it has been observed that there is a significant positive correlation between the expression of MIEN1 and CRNDE. In contrast, miR-136-5p expression in GC tissues shows a negative correlation. Conclusion: A previously unexplored therapeutic target for GC involves the CRNDE/miR-136-5p/MIEN1 signal transduction cascade.

BACKGROUND: MiR-136-5p plays a vital function in regulating developmental processes as well as in the pathophysiology of diseases, with a notable record in tumor suppression.
METHODS: This article summarizes the latest findings on the physiological and pathophysiological processes of miR-136-5p in diseases. We searched for relevant studies and selected research articles from the last five years on PubMed with miR-136-5p as the keyword.
RESULTS: MiR-136-5p represents a class of microRNAs (miRNAs) that are involved in various human maladies, encompassing cancers, cardio-cerebrovascular disease, diabetes, inflammatory disease, tuberous sclerosis, idiopathic pulmonary fibrosis, and polycystic ovary syndrome. Altered expression of miR-136-5p in specific ailments results in downstream gene expression imbalance, influencing cellular behaviors, such as migration, proliferation, and invasion. Furthermore, miR-136-5p is implicated in five signaling pathways, where it is critical in the onset and advancement of a number of illnesses. Additionally, it has the potential to promote drug resistance to a variety of medications.
CONCLUSIONS: The current review aims to elucidate the role of miR-136-5p in both cancer progression and non-cancerous disorders, emphasizing dysregulated signaling pathways. It also sheds light on the potential of this miRNA as a prognostic biomarker in cancer, offering valuable insights and directions for future research.

MicroRNAs (miRNAs) have emerged as important regulators of gene expression, and the deregulation of their activity has been linked to the onset and progression of a variety of human malignancies. Among these miRNAs, miR-136-5p has attracted significant attention due to its diverse roles in cancer biology. Mostly, miR-136-5p is downregulated in malignancies. It could inhibit viability, proliferation, migration, invasion and promote apoptosis of tumor cells. This review article provides a comprehensive overview of the current understanding of miR-136-5p in different sorts of human cancers: genital tumors, head and neck tumors, tumors from the digestive and urinary systems, skin cancers, neurologic tumors, pulmonary neoplasms and other cancers by discussing its molecular mechanisms, functional roles, and impact in chemotherapies. In conclusion, miR-136-5p could be a promising new biomarker and potential clinical therapeutic target.

Nasopharyngeal carcinoma (NPC) features high mortality and poor prognosis. Additionally, long non-coding RNAs (lncRNAs) play a significant role in developing NPC and other types of cancer. But the functional mechanism of MIR100HG in NPC remains unclear. The long non-coding RNA MIR100HG messenger RNA (mRNA) expression was thoroughly evaluated in NPC tumors and adjacent tissues using quantitative polymerase chain reaction (qPCR). Furthermore, we employed Kaplan-Meier analysis to compare the expression of MIR100HG with survival outcomes. The CCK8 test was utilized to investigate the impact of the lncRNA MIR100HG/miR-136-5p/IL-6 axis on cell proliferation in NPC. The study\'s findings indicated overexpression of the lncRNA MIR100HG in both NPC tumors and cell lines. This upregulation was associated with a poorer outcome in individuals with NPC. When lncRNA MIR100HG was knocked down in vitro, NPC cell proliferation was inhibited, resulting in tumor suppression. In certain oncogenic capacities, the lncRNA MIR100HG functions as a competitive endogenous RNA for miR-136-5p, hence impeding the inhibitory effect of miR-136-5p on its target gene, IL-6. In summary, the findings of the present investigation suggested that lncRNA MIR100HG exhibits promising characteristics as a potential indicator for the prognosis and diagnosis of NPC.

A handful of circular RNAs (circRNAs) associated with cancer progression have been indicated in esophageal squamous cell carcinoma (ESCC). The current study aimed to investigate the functional mechanism of circular RNA Fibronectin type III domain containing 3B (circ_FNDC3B) in ESCC. Circ_FNDC3B, FNDC3B, microRNA-136-5p (miR-136-5p) and mitogen-activated protein kinase 1 (MAPK1) were examined via the quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8) and colony formation assays. Transwell assay was performed to measure cell migration and invasion. Protein analysis was implemented by western blot. Cell apoptosis was assessed via flow cytometry. Target interaction was affirmed using dual-luciferase reporter assay. The function analysis of circ_FNDC3B in vivo was explored by xenograft models. The upregulation of circ_FNDC3B was detected in ESCC tissues and cells. Functionally, ESCC cell proliferation and metastasis were repressed but apoptosis was promoted by circ_FNDC3B knockdown. Besides, circ_FNDC3B silence inhibited ESCC progression through MAPK1 downregulation. Further target analysis identified miR-136-5p as a target of circ_FNDC3B and an upstream control of MAPK1. Additionally, the regulation of si-circ_FNDC3B in ESCC was also dependent on targeting miR-136-5p. Moreover, circ_FNDC3B targeted miR-136-5p to affect MAPK1 level. Tumorigenesis in vivo was also suppressed by downregulating circ_FNDC3B to regulate miR-136-5p/MAPK1 axis. Circ_FNDC3B downregulation impeded the development of ESCC via the mediation of miR-136-5p/MAPK1 axis. This report afforded a novel insight into the functional mechanism of circ_FNDC3B in ESCC.

BACKGROUND: Colorectal cancer (CRC) is a common gastrointestinal malignancy. Dysregulation of circular RNAs (circRNAs) is associated with the progression of CRC. However, the role of circ_0013339 (hsa_circ_0013339) in CRC is still not clear.
METHODS: The levels of circ_0013339, miR-136-5p, and SRY-box transcription factor 9 (SOX9) in CRC were gauged by quantitative real-time polymerase chain reaction (qRT-PCR). Colony formation and 5-Ethynyl-2\'-deoxyuridine (EdU) assays were used to detect cell proliferation. Cell counting kit-8 (CCK8) assay was used to measure cell viability. Western blot assay was performed to examine protein expression. The relationship between miR-136-5p and circ_0013339 or SOX9 was tested by dual-luciferase reporter assay. The effect of sh-circ_0013339 on tumor growth in vivo was examined by xenograft experiments.
RESULTS: Circ_0013339 expression was elevated in CRC tissues and cells, and circ_0013339 knockdown diminished the growth of CRC cells. MiR-136-5p was regulated by circ_0013339. MiR-136-5p deficiency ameliorated the effects of circ_0013339 silencing on CRC cell malignant behaviors. Circ_0013339 modulated SOX9 expression through miR-136-5p. SOX9 addition reversed the effects of miR-136-5p overexpression on CRC cell behaviors. Moreover, silencing of circ_0013339 suppressed the growth of xenograft tumors in vivo.
CONCLUSIONS: Circ_0013339 regulates the progression of CRC through miR-136-5p-dependent regulation of SOX9, uncovering a novel regulatory mechanism of circ_0013339 in CRC.

The involvement of circular RNAs (circRNAs) in laryngeal squamous cell carcinoma (LSCC) carcinogenesis has gradually been proposed. Herein, we aimed to explore the function and mechanism of circPRRC2C in LSCC. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were used for detecting the content of genes and proteins. In vitro experiments were conducted using 5-ethynyl-2\'-deoxyuridine, colony formation, flow cytometry, and transwell assays. The binding between miR-136-5p and circPRRC2C or Homeobox D11 (HOXD11) was confirmed by using the dual-luciferase reporter assay. The murine xenograft model was established for in vivo analysis. The commercial kit was used for exosome separation. CircPRRC2C is a stable circRNA, and was highly expressed in LSCC tissues and cell lines. Functionally, circPRRC2C deficiency impaired LSCC cell proliferation, migration and invasion but induced cell apoptosis in vitro and impeded tumor growth in vivo, however, circPRRC2C overexpression showed the exact opposite effects. Mechanistically, circPRRC2C directly targeted miR-136-5p, which showed inhibitory effects on the growth and mobility of LSCC cells. Meanwhile, miR-136-5p directly targeted HOXD11, and circPRRC2C/miR-136-5p/HOXD11 formed a feedback loop in LSCC cells. Further rescue assays exhibited that circPRRC2C exerted its effects by miR-136-5p/HOXD11 axis. In addition, circPRRC2C was stably packaged into exosomes and showed potential diagnostic value for LSCC. CircPRRC2C acted as an oncogene to promote LSCC cell oncogenic phenotypes via miR-136-5p/HOXD11 axis, besides, circPRRC2C was stably packaged into exosomes, indicating the potential application of circPRRC2C-targeting agents in the treatment in LSCC.

The biological functions of circTLK1 in acute kidney injury (AKI), which mainly results from renal ischemia-reperfusion (IR), remain largely unknown. HK-2 cell treatment with oxygen and glucose deprivation, reoxygenation, and glucose (OGD/R) was used to simulate an AKI model that was mainly caused by renal IR. Then, the circTLK1 expression level in HK-2 cells treated with OGD/R was assessed by quantitative reverse transcription polymerase chain reaction (RT-qPCR). Functional experiments were performed with circTLK1 knockdown of HK-2 cells via Cell Counting Kit-8 (CCK8), flow cytometry (FCM), RT-qPCR, and western blotting. The circTLK1-miRNAs-mRNAs network was constructed following the ceRNA mechanism and visualized by Cytoscape software to investigate the mechanism of circTLK1 in AKI. RT-qPCR was performed to verify the relationship between circTLK1, miR-136-5p, and Bcl2. The level of miR-136-5p was knocked down to ensure its function in OGD/R-triggered apoptosis through experiments, including CCK8, FCM, RT-qPCR, and western blotting. CircTLK1 was downregulated in HK-2 cells subjected to OGD/R treatment and in mouse kidney tissues after renal IR, but the expression of miR-136-5p was the opposite. Interference with circTLK1 expression accelerated HK-2 cell apoptosis, which was overturned by miR-136-5p inhibitors. CircTLK1 targets miR-136-5p to upregulate Bcl2 expression and attenuate apoptosis in HK-2 cells. These data revealed the possible role of circTLK1 as a new biomarker for diagnosis as well as a target in AKI through the miR-136-5p/Bcl2 signaling axis.

Known as long non-coding RNAs (lncRNAs), they are essential in regulating tumour metastasis. In gastric carcinoma (GC), lncRNA cytoskeleton regulator (CYTOR) keeps at high levels, but its influences on GC cell proliferation, migration and invasion need further investigation. Hence, the role played by lncRNA CYTOR in GC was explored in this study. We employed quantitative reverse transcription PCR (RT-qPCR) to determine lncRNA CYTOR and microRNA (miR)-136-5p levels in GC, Western blot analysis to measure Homeobox C10 (HOXC10), and Flow cytometry, transwell, and cell counting kit-8 (CCK-8) assays to evaluate the roles played by miR-136-5p and lncRNA CYTOR in GC cells. Furthermore, bioinformatics analysis and Luciferase assay were carried out to identify the target genes of the two. LncRNA CYTOR was found to be upregulated in GC cells, and its knockdown inhibited GC cell growth. MiR-136-5p, underexpressed in GC cells, was identified as a target of CYTOR in modulating GC progression. Moreover, HOXC10 was miR-136-5p\'s downstream target. Finally, CYTOR participated in GC progression in vivo. Collectively, CYTOR modulates the miR-136-5p/HOXC10 axis to accelerate GC progression.