[Corrigendum] Linc00961 inhibits the proliferation and invasion of skin melanoma by targeting the miR­367/PTEN axis.

Following the publication of the above article, the authors have informed us that they found errors in two of the published figures that occurred whilst compiling them. In Fig. 8, the representative images selected for the migratory and invasive A375 cells in the Lv­control + miR­367 NC group experiments were found to be overlapping. After having consulted their original data, the authors noted that the error arose during the data acquisition process, and an area of the image captured for the migratory A375 cells was inadvertently re­used as the invasive A375 cells for the Lv­control + miR­367 NC group. Likewise, in Fig. S3, the error arose during the process of assembling the data in the figure: In this case, the (A) migratory and (B) invasive cell images shown for the SK­MEL­28/Lv­LINC00961 + PTEN siRNA experiments were selected incorrectly. The revised versions of Figs. 8 and S3 are shown on the next page. The authors regret that these errors went unnoticed prior to publication, and thank the Editor of International Journal of Oncology for allowing them this opportunity to publish this corrigendum. All the authors agree with the publication of this corrigendum; furthermore, they also apologize to the readership of the journal for any inconvenience caused. [the original article was published in International Journal of Oncology 55: 708­720, 2019; DOI: 10.3892/ijo.2019.4848].

Linc00961 inhibits the proliferation and invasion of skin melanoma by targeting the miR­367/PTEN axis.

Long intergenic noncoding RNA 00961 (Linc00961) has been identified as a tumor suppressor in various types of cancer. However, the critical roles of Linc00961 in the carcinogenesis and progression of skin melanoma (SM) are yet to be fully elucidated. The present study revealed via reverse transcription­quantitative PCR analysis that Linc00961 was downregulated in the tissues of patients with SM compared with benign nevi, and in A375, A2058 and SK­MEL­28 cell lines compared with human melanocytes. Furthermore, overexpression of Linc00961 inhibited cell proliferation, and promoted the apoptosis of A375 and SK­MEL­28 cells in vitro and in vivo, as determined by Cell Counting Kit­8 and flow cytometry assays, and tumor xenograft studies, respectively. Overexpression of Linc00961 also led to an attenuation of the migration and invasive capabilities of A375 and SK­MEL­28 cells, measured using Transwell assays. Functionally, it was demonstrated that Linc00961 acted as a competing endogenous RNA (ceRNA) by competitively sponging microRNA­367 (miR­367) in A375 and SK­MEL­28 cells; restoration of miR­367 rescued the inhibitory effects of Linc00961 on A375 and SK­MEL­28 cells. Finally, it was observed that phosphate and tension homology deleted on chromosome 10 (PTEN), an established target of miR­367 in A375 and SK­MEL­28 cells, was positively regulated by Linc00961, and its inhibition reversed the inhibitory effects of Linc00961 on the proliferation and invasion of A375 and SK­MEL­28 cells. Collectively, the present study revealed that Linc00961 was downregulated in SM, and furthermore, Linc00961 was identified as a ceRNA that inhibits the proliferation and invasion of A375 and SK­MEL­28 cells by modulating the miR­367/PTEN axis.

[Effects of 8-Methoxypsoralen on intracellular [Ca(2+)]i and cytoskeleton actin organization in human melanocytes in vitro].

OBJECTIVE: To investigate the effects of 8-methoxypsoralen on human melanocytes [Ca(2+)]i and cytoskeleton actin organization in vitro. METHODS: Human melanocytes were obtained from normal foreskins. Laser confocal microscope was employed to measure [Ca(2+)]i and rhodamine-conjugated phalloidin was used to visualize the cytoskeleton actin. RESULTS: 8-methoxypsoralen increased [Ca(2+)]i and induced organization of actin stress fiber cytoskeleton. CONCLUSION: 8-methoxypsoralen might influence the migration of melanocytes by increasing the intracellular free Ca(2+) concentration and cytoskeleton actin reorganization.

[Effects of bFGF and alpha-MSH on adhesion and migration of human melanocytes in vitro].

OBJECTIVE: To observe the effect of basic fibroblast growth factor (bFGF) and alpha-melanocyte stimulating hormone (alpha-MSH) on adhesion and migration of melanocytes in vitro. METHODS: Human melanocytes were obtained from normal human foreskins. Culture dishes covered with fibronectin were used to perform melanocytes adhesion assay, and cell motility was assessed using the Transwell micropore filter method. RESULT: bFGF and alpha-MSH increased melanocytes adhesion on culture dishes covered with fibronectin. bFGF stimulated melanocytes migration through micropore filter while alpha-MSH had no significant effects. CONCLUSION: bFGF and alpha-MSH could promote the adhesion and migration of melanocytes, which suggests that two agents may play a role in the repigmentation of vitiligo.

[Effects of MSF on melanocyte adhesion and migration in vitro].

OBJECTIVE: To investigate the Malytea Scurfpea fruit (MSF) on melanocyte adhesion and migration. METHOD: Human epidermal melanocytes were treated with MSF and Ginger respectively, then adhesion to bovine serum fibronectin-coated culture dishes was checked. Control and treated cells were also examined for migration into micropore filters coated with the same protein. RESULT: Compared with control, MSF treated melanocytes were obviously easier to adhere to the dishes and move into the filters in a dose-dependent manner. When the dose of MSF was 200 mg x L(-1), it could not reincrease melanocyte adhesion and migration. At 10 mg x L(-1), under every other concentrations of MSF, there was no marked difference among MSF-treated, Ginger-treated and untreated melanocytes (P < 0.05) when adhesion test were studied. But to migration, even at 10 mg x L(-1) MSF, there was obvious increased migration compared with MSF-untreated or Ginger-treated melanocytes (P < 0.01). CONCLUSION: MSF has effect on melanocyte adhesion and migration, which can explain, in part, the capacity of MSF to modulate melanocyte function in vitiligo lesions.

Effects of endothelin-1 on melanocyte adhesion and migration.

OBJECTIVE: To investigate the effect of endothelin-1 (ET-1) on the adhesion and migration of melanocyte in vitro. METHODS: Human epidermal melanocytes that had been cultured and purified were treated with ET-1 and observed for adhesion to bovine serum fibronectin-coated culture dishes. Stem cell factor (SCF) and ET-1 treated cells were also examined for migration into micropore filters coated with the same protein. RESULTS: Compared with the SCF group, ET-1 treated melanocytes were easier to adhere to the dishes and to be moved into the filters, especially when the concentration was 32 nmol/L. When the concentration of ET-1 was 128 nmol/L or more, it could inhibit the adhesion and migration of melanocyte. At any concentration of ET-1 except at 2 nmol/L, there was a significant difference between ET-1-treated and untreated melanocytes (P < 0.01) when the adhesion test was carried out. However, even at 2 nmol/ L ET-1, there was obviously increased migration compared with those of ET-1 untreated melanocytes and SCF-treated cells (P < 0.01). CONCLUSION: ET-1 may influence the adhesion and migration of melanocyte, which can partly explain the capacity of ET-1 to regulate the melanocyte function in vitiligo lesions.