miRNA-144 suppresses proliferation and migration of colorectal cancer cells through GSPT1

miR-142-3p Suppresses Cell Growth by Targeting CDK4 in Colorectal Cancer

“…Moreover, compelling evidence indicates that miRNAs may play important roles in CRC progression and may directly contribute to the proliferation, avoidance of apoptosis and metastasis of CRC [20,21]. MiR-103 is an oncogene miRNA that promotes colorectal cancer proliferation and migration through downregulation of the tumor suppressor genes DICER and PTEN [22]; miR-204-5p acts as a tumor suppressor in colorectal cancer through inhibiting RAB22A [23]; miR-144 was markedly down-regulated in colorectal cancer and can inhibit the proliferation and migration of [24]; the IL-6R/STAT3/miR-34a loop was necessary for EMT, invasion, and metastasis of CRC cell lines [25]; miR-378 expression was low in colon cancer tissues and cell lines and miR-378 not only inhibits the proliferation of colon cancer cells in vitro by inducing apoptosis, but also inhibits migration and invasion by inhibiting the EMT of colon cancer cells [26]; miR-153 was highly expressed in a cellular model of advanced stage colorectal cancer and increased colorectal cancer invasiveness and resistance to oxaliplatin and cisplatin [27]; miR-451 was over-expressed in multiple colorectal cancer tissues and might inhibit AMPK to activate mTORC1, which mediates FSCN1 expression and cancer cell progression [28]. miR-142 is expressed in many other tissues and displays a functional role in cancer, virus infection, inflammation and immune tolerance [29].…”

Profile of Expression of Genes Encoding Matrix Metallopeptidase 9 (MMP9), Matrix Metallopeptidase 28 (MMP28) and TIMP Metallopeptidase Inhibitor 1 (TIMP1) in Colorectal Cancer: Assessment of the Role in Diagnosis and Prognostication

“…This relationship is very complex in CRC, which results from the changeable activity of genes encoding these mediators [34]. Xiao et al [35] demonstrated that miRNA-144 (suppressed by the expression of GSPT1) may be the connecting element to regulate the expression of Survivin, thereby inhibiting MMP28.…”

The features of KRAS gene transcriptional activity and significance in colorectal cancer

“…Таким чином, зниження рівня проліферативної активності в ході прогресії КРА від I до IV стадій її розвитку, найімовірніше, опосередковується залученням інших шляхів сигналізації, не пов'язаних з RASпротеїном. Було знайдено публікації, в яких наведено механізм пригнічення проліферації ракових клітин КРА за рахунок регуляторного впливу окремих сімейств мікроРНК [14,16,18], а також дані, згідно з якими зниження проліферативної активності пухлинних клітин КРА асоціюється з активацією механізмів, що запускають епітеліально-мезенхімальну трансформацію [12].…”