hsa_circ_0000285 facilitates thyroid cancer progression by regulating miR‐127‐5p/CDH2

Abstract

Thyroid cancer (THCA) is a leading endocrine cancer and becomes the fifth most commonly diagnosed malignancy in females. It is confirmed that circular RNAs (circRNAs) perform regulatory potencies in the pathological progress of THCA. Our purpose was to certify the trait of hsa_circ_0000285 (circ_0000285) and investigate its modulatory mechanism in THCA progression. We identified the expression profile of hsa_circ_0000285 in THCA by conducting qRT‐PCR assay. Therewith, the potential of hsa_circ_0000285 in THCA development was determined with a set of functional experiments, including CCK‐8, wound healing assay, Western blot, and xenograft model. The molecular mechanism underlying hsa_circ_0000285 was investigated with bioinformatic analysis, RIP and dual‐luciferase reporter experiments. As opposed to normal samples and cells, hsa_circ_0000285 level was overtly increased in THCA specimens and cells. The downregulation of hsa_circ_0000285 weakened the proliferative and migratory capacity of THCA cells and promoted cell apoptosis. In addition, hsa_circ_0000285 silence suppressed the tumor growth of xenograft model mice in vivo. Notably, we demonstrated that hsa_circ_0000285 might target miR‐127‐5p/CDH2 axis in THCA. Afterward, our findings manifested that miR‐127‐5p attenuation blocked the function of hsa_circ_0000285 depletion in THCA cells. In the final step, CDH2 was proven to mediate the repressive potency of miR‐127‐5p in the malignant behaviors of THCA. Mechanistically, hsa_circ_0000285 induced the development of THCA via functioning as a competing endogenous RNA (ceRNA) of miR‐127‐5p to enhance CDH2 expression, which provided a new perspective for THCA therapy.

miR-127-5p regulates FAIM2-mediated cell apoptosis and participates in cerebral ischemia-reperfusion injury

“…To further analyze the function of miR-127-5p in CI/RI, OGD/R-treated cells were interfered with miR-127-5p inhibition, contributing to the promotion of proliferation and the suppression of apoptosis and death. miR-127-5p has been defined as a tumor suppressor [25][26][27] that is associated with the malignant progression of tumor growth. Additionally, studies have shown the regulatory involvement of miR-127-5p in osteoarthritis in part by controlling apoptosis and proliferation of chondrocytes [28][29][30].…”

Using ncRNAs as Tools in Cancer Diagnosis and Treatment—The Way towards Personalized Medicine to Improve Patients’ Health

“…In several types of cancer, most lncRNAs are either up- or downregulated. These lncRNAs favor all stages of tumor development through the promotion of mRNA expression and constancy [ 253 ], by favoring mRNA stability [ 254 ], or by modulating miR [ 254 , 255 , 256 , 257 , 258 , 259 , 260 , 261 , 262 , 263 , 264 , 265 , 266 , 267 , 268 , 269 , 270 , 271 , 272 , 273 , 274 , 275 , 276 , 277 , 278 , 279 , 280 , 281 , 282 , 283 , 284 , 285 , 286 , 287 , 288 , 289 , 290 , 291 , 292 , 293 , 294 , 295 , 296 , 297 , 298 , 299 , 300 ]. The aberrant phenotype is the result of the modulation of typical pathways playing key roles in cell survival [ 255 , 259 , 263 , 265 , 283 ], apoptosis [ <...…”

“…Another important pathway in cancer is the phosphoinositide 3-kinase-AKT-mammalian target of the rapamycin (PI3K-AKT-mTOR) pathway, which is frequently hyperactivated in cancer and is essential for tumor cell growth and survival [ 61 ]. Indeed, several lncRNAs such as HOTAIR, HOXD-AS1, LINC00511, H19, and LINC01554, by targeting specific miRs, increase the expression of AKT and mTOR, promoting aberrant phenotypes [ 262 , 264 , 271 , 274 , 278 , 287 , 296 ].…”

Calycosin Inhibits Pancreatic Cancer Cell Proliferation, Migration and Invasion by Repressing Circ_0000285

“…Unlike other non-coding RNAs, circular RNAs (circRNAs) have covalently closed loop structure produced by the back-spliced mechanism of pre-messenger RNA (mRNA), which are abnormally expressed in numerous tumors and partake in the process of tumorigenesis and development [11] . Previous studies have indicated that circ_0000285 acted as a well-known carcinogenic factor in various human cancers [12,13] , but its role in pancreatic cancer has not been reported. Accordingly, this project focused on whether CC might control pancreatic cancer progression via modulating circ_0000285.…”