These results suggest that the three miRNAs are negative regulators of Fus1 expression in lung cancers.

Data suggest that miR-98 (and miR-453) down-regulates TP53 expression by targeting the 3-prime-UTR of TP53 in lung cancer cells.

Study showed that NEAT1 could function as a competing endogenous lncRNA in lung cancer, mediating CTR1 by sponging hsa-mir-98-5p.

Peripheral B cells express less miR-98 in patients with lung cancer.A negative correlation was identified between miR-98 and IL-10 in peripheral B cells.

MiR-98 acts as a tumor suppressor in non-small cell lung cancer cells by inhibiting the protein expression of its target gene SALL4.

NEAT1/hsa-mir-98-5p/MAPK6 is involved in the development and progress in non-small-cell lung cancer.

Results show that miR98 is downregulated in nonsmall cell lung cancer (NSCLC) and associated with progression. Its downregulation enhances the viability, proliferation, migration and invasion. miR985p significantly suppressed tumor metastasis in a mouse model of pulmonary metastasis.

findings demonstrate that SNHG4 is required by lung cancer cells to maintain malignant phenotype; SNHG4 probably exerts its pro-survival and pro-metastatic effects by sponging anti-tumor miR-98-5p

ALG3 contributes to the malignancy of non-small cell lung cancer and is negatively regulated by MiR-98-5p.

Knockdown of lncRNA ANRIL inhibits the development of cisplatin resistance by upregulating miR98 in lung cancer cells.